Fine Particulate Matter Exposure Research Articles

Increase in sick leave episodes from short-term fine particulate matter exposure: A case-crossover study in Stockholm, Sweden

Air pollution's short-term effects on a wide range of health outcomes have been studied extensively, primarily focused on vulnerable groups (e.g., children and the elderly). However, the air pollution effects on the adult working population through sick leave have received little attention. This study aims to 1) estimate the associations between particulate matter ≤2.5 μm3 (PM2.5) and sick leave episodes and 2) calculate the attributable number of sick leave days and the consequential productivity loss in the City of Stockholm, Sweden.Individual level daily sick leave data was obtained from Statistics Sweden for the years 2011–2019. Daily average concentrations of PM2.5 were obtained from the main urban background monitoring station in Stockholm. A case-crossover study design was applied to estimate the association between short-term PM2.5 and onset of sick leave episodes. Conditional logistic regression was used to estimate the relative increase in odds of onset per 10 μg/m3 of PM2.5, adjusting for temperature, season, and pollen. A human capital method was applied to estimate the PM2.5 attributable productivity loss.In total, 1.5 million (M) individual sick leave occurrences were studied. The measured daily mean PM2.5 concentration was 4.2 μg/m3 (IQR 3.7 μg/m3). The odds of a sick leave episode was estimated to increase by 8.5% (95% CI: 7.8–9.3) per 10 μg/m3 average exposure 2–4 days before. Sub-group analysis showed that private sector and individuals 15–24 years old had a lower increase in odds of sick leave episodes in relation to PM2.5 exposure. In Stockholm, 4% of the sick leave episodes were attributable to PM2.5 exposure, corresponding to €17 M per year in productivity loss.Our study suggests a positive association between PM2.5 and sick leave episodes in a low exposure area.

Reduction of Outdoor and Indoor PM2.5 Source Contributions via Portable Air Filtration Systems in a Senior Residential Facility in Detroit, Michigan.

Background: The Reducing Air Pollution in Detroit Intervention Study (RAPIDS) was designed to evaluate cardiovascular health benefits and personal fine particulate matter (particulate matter < 2.5 μm in diameter, PM2.5) exposure reductions via portable air filtration units (PAFs) among older adults in Detroit, Michigan. This double-blind randomized crossover intervention study has shown that, compared to sham, air filtration for 3 days decreased 3-day average brachial systolic blood pressure by 3.2 mmHg. The results also showed that commercially available HEPA-type and true HEPA PAFs mitigated median indoor PM2.5 concentrations by 58% and 65%, respectively. However, to our knowledge, no health intervention study in which a significant positive health effect was observed has also evaluated how outdoor and indoor PM2.5 sources impacted the subjects. With that in mind, detailed characterization of outdoor and indoor PM2.5 samples collected during this study and a source apportionment analysis of those samples using a positive matrix factorization model were completed. The aims of this most recent work were to characterize the indoor and outdoor sources of the PM2.5 this community was exposed to and to assess how effectively commercially available HEPA-type and true HEPA PAFs were able to reduce indoor and outdoor PM2.5 source contributions. Methods: Approximately 24 h daily indoor and outdoor PM2.5 samples were collected on Teflon and Quartz filters from the apartments of 40 study subjects during each 3-day intervention period. These filters were analyzed for mass, carbon, and trace elements. Environmental Protection Agency Positive Matrix Factorization (PMF) 5.0 was utilized to determine major emission sources that contributed to the outdoor and indoor PM2.5 levels during this study. Results: The major sources of outdoor PM2.5 were secondary aerosols (28%), traffic/urban dust (24%), iron/steel industries (15%), sewage/municipal incineration (10%), and oil combustion/refinery (6%). The major sources of indoor PM2.5 were organic compounds (45%), traffic + sewage/municipal incineration (14%), secondary aerosols (13%), smoking (7%), and urban dust (2%). Infiltration of outdoor PM2.5 for sham, HEPA-type, and true HEPA air filtration was 79 ± 24%, 61 ± 32%, and 51 ± 34%, respectively. Conclusions: The results from our study showed that intervention with PAFs was able to significantly decrease indoor PM2.5 derived from outdoor and indoor PM2.5 sources. The PAFs were also able to significantly reduce the infiltration of outdoor PM2.5. The results of this study provide insights into what types of major PM2.5 sources this community is exposed to and what degree of air quality and systolic blood pressure improvements are possible through the use of commercially available PAFs in a real-world setting.

Indoor and Personal PM2.5 Samples Differ in Chemical Composition and Alter Zebrafish Behavior Based on Primary Fuel Source.

Fine particulate matter (PM2.5) exposure has been linked to diverse human health impacts. Little is known about the potential heterogeneous impacts of PM2.5 generated from different indoor fuel sources and how exposure differs between personal and indoor environments. Therefore, we used PM2.5 collected by one stationary sampler in a kitchen and personal samplers (female and male participants), in homes (n = 24) in Kheri, India, that used either biomass or liquified petroleum gas (LPG) as primary fuel sources. PM2.5 samples (pooled by fuel type and monitor placement) were analyzed for oxidative potential and chemical composition, including elements and 125 organic compounds. Zebrafish (Danio rerio) embryos were acutely exposed to varying concentrations of PM2.5 and behavioral analyses were conducted. We found relatively high PM2.5 concentrations (5-15 times above World Health Organization daily exposure guidelines) and varied human health-related chemical composition based on fuel type and monitor placement (up to 15% carcinogenic polycyclic aromatic hydrocarbon composition). Altered biological responses, including changes to mortality, morphology, and behavior, were elicited by exposure to all sample types. These findings reveal that although LPG is generally ranked the least harmful compared to biomass fuels, chemical characteristics and biological impacts were still present, highlighting the need for further research in determining the safety of indoor fuel sources.

Fine particulate matter (PM2.5) exposure assessment among active daily commuters to induce behaviour change to reduce air pollution

Fine particulate matter (PM2.5), a detrimental urban air pollutant primarily emitted by traffic and biomass burning, poses disproportionately significant health risks at relatively limited exposure during commuting. Previous studies have mainly focused on fixed locations when assessing PM2.5 exposure, while neglecting pedestrians and cyclists, who often experience higher pollution levels. In response, this research aimed to independently validate the effectiveness of bicycle-mounted low-cost sensors (LCS) adopted by citizens, evaluate temporal and spatial PM2.5 exposure, and assess associated health risks in Ljubljana, Slovenia. The LCS quality assurance results, verified by co-location field tests by air quality monitoring stations (AQMS), showed comparable outcomes with an average percentage difference of 21.29 %, attributed to humidity-induced nucleation effects. The colder months exhibited the highest air pollution levels (μ = 32.31 μg/m3) due to frequent thermal inversions and weak wind circulation, hindering vertical air mixing and the adequate dispersion of pollutants. Additionally, PM2.5 levels in all sampling periods were lowest in the afternoon (μ = 12.09 μg/m3) and highest during the night (μ = 61.00 μg/m3) when the planetary boundary layer thins, leading to the trapping of pollutants near the surface, thus significantly affecting diurnal and seasonal patterns. Analysis of exposure factors revealed that cyclists were approximately three times more exposed than pedestrians. However, the toxicological risk assessment indicated a minimal potential risk of PM2.5 exposure. The collaborative integration of data from official AQMS and LCS can enhance evidence-based policy-making processes and facilitates the realignment of effective regulatory frameworks to reduce urban air pollution.

Prenatal exposure to fine particulate matter chemical constituents and the risk of stillbirth and the mediating role of pregnancy complications: A cohort study

Evidence on the association of fine particulate matter (PM2.5) exposure with stillbirth is limited and inconsistent, which is largely attributed to differences in PM2.5 constituents. Studies have found that the hazards of certain PM2.5 constituents to the fetus are comparable to or even higher than total PM2.5 mass. However, few studies have linked PM2.5 constituents to stillbirth. Moreover, the mediating role of pregnancy complications in PM2.5-related stillbirth remains unclear. To our knowledge, this study was the first to explore the individual and mixed associations of PM2.5 and its constituents with stillbirth in China. After matching the concentrations of PM2.5 and its constituents (sulfate [SO42−], nitrate [NO3−], ammonium [NH4+], organic matter [OM], and black carbon [BC]) for participants according to their geographical location, there were 170,507 participants included in this study. We found that stillbirth was associated with exposure to PM2.5 and its constituents in the year before pregnancy and during the entire pregnancy, and the associations in trimester 1 were strongest. The risk of stillbirth increased sharply when PM2.5 and its constituents during pregnancy exceeded the median concentrations. Moreover, stillbirth was associated with exposure to the mixtures of SO42−, NO3−, NH4+, OM, and BC before and during pregnancy (trimesters 1 and 2). Meanwhile, two-pollutant models also suggested stillbirth was associated with PM2.5 and its constituents in the year before and during pregnancy. The associations of PM2.5 and its constituents with stillbirth were stronger in mothers with advanced age and without cesarean delivery history. Additionally, hypertensive disorders in pregnancy, gestational diabetes, and placental abruption mediated the association of PM2.5 with stillbirth. Therefore, enhanced protection against PM2.5 for pregnant women before and during pregnancy and targeted interventions for pregnancy complications and anthropogenic sources of PM2.5 constituents are important to reduce stillbirth risk.

Associations between weekly gestational exposure of fine particulate matter, ozone, and nitrogen dioxide and preterm birth in a North Carolina Birth Cohort, 2003-2015.

Preterm birth (PTB; <37 weeks completed gestation) is associated with exposure to air pollution, though variability in association magnitude and direction across exposure windows exists. We evaluated associations between weekly gestational exposure to fine particulate matter (PM2.5), nitrogen dioxide (NO2), and ozone (O3) with PTB in a North Carolina Birth Cohort from 2003 to 2015 (N = 1,367,517). Daily average PM2.5 and daily 8-hour maximum NO2 concentration estimates were obtained from a hybrid ensemble model with a spatial resolution of 1 km2. Daily 8-hour maximum census tract-level concentration estimates for O3 were obtained from the EPA's Fused Air Quality Surface Using Downscaling model. Air pollutant concentrations were linked by census tract to residential address at delivery and averaged across each week of pregnancy. Modified Poisson regression models with robust errors were used to estimate risk differences (RD [95% confidence intervals (CI)]) for an interquartile range increase in pollutants per 10,000 births, adjusted for potential confounders. Associations were similar in magnitude across weeks. We observed positive associations for PM2.5 and O3 exposures, but generally null associations with NO2. RDs ranged from 15 (95% CI = 11, 18) to 32 (27, 37) per 10,000 births for PM2.5; from -7 (-14, -1) to 0 (-5, 4) for NO2; and from 4 (1, 7) to 13 (10, 16) for O3. Our results show that increased PM2.5 exposure is associated with an increased risk of PTB across gestational weeks, and these associations persist in multipollutant models with NO2 and/or O3.

Fine Particulate Matter Exposure, Genetic Susceptibility, and the Risk of Incident Stroke: A Prospective Cohort Study.

Both genetic factors and environmental air pollution contribute to the risk of stroke. However, it is unknown whether the association between air pollution and stroke risk is influenced by the genetic susceptibilities of stroke and its risk factors. This prospective cohort study included 40 827 Chinese adults without stroke history. Satellite-based monthly fine particulate matter (PM2.5) estimation at 1-km resolution was used for exposure assessment. Based on 534 identified genetic variants from genome-wide association studies in East Asians, we constructed 6 polygenic risk scores for stroke and its risk factors, including atrial fibrillation, blood pressure, type 2 diabetes, body mass index, and triglyceride. The Cox proportional hazards model was applied to evaluate the hazard ratios and 95% CIs for the associations of PM2.5 and polygenic risk score with incident stroke and the potential effect modifications. Over a median follow-up of 12.06 years, 3147 incident stroke cases were documented. Compared with the lowest quartile of PM2.5 exposure, the hazard ratio (95% CI) for stroke in the highest quartile group was 2.72 (2.42-3.06). Among individuals at high genetic risk, the relative risk of stroke was 57% (1.57; 1.40-1.76) higher than those at low genetic risk. Although no statistically significant interaction was found, participants with both the highest PM2.5 and high genetic risk showed the highest risk of stroke, with ≈4× that of the lowest PM2.5 and low genetic risk group (hazard ratio, 3.55 [95% CI, 2.84-4.44]). Similar upward gradients were observed in the risk of stroke when assessing the joint effects of PM2.5 and genetic risks of blood pressure, type 2 diabetes, body mass index, atrial fibrillation, and triglyceride. Long-term exposure to PM2.5 was associated with a higher risk of incident stroke across different genetic susceptibilities. Our findings highlighted the great importance of comprehensive assessment of air pollution and genetic risk in the prevention of stroke.

On the short-term impact of pollution: The effect of PM 2.5 on emergency room visits.

In this paper, we study the short-term effect of fine particulate matter (PM 2.5) exposure on respiratory emergency room (ER) visits in Chile, a middle-income country with high levels of air pollution. To instrument for PM 2.5, we use wind speed at different altitudes (pressure levels). Unlike previous papers, our data allow us to study the impact of high pollution levels across all age groups. We find that a 1μg per cubic meter (μg/m3 ) increase in PM 2.5 exposure for 1day increases ER visits for respiratory illness by 0.36%. The effect is positive and significant for all age groups. Furthermore, the coefficients on government environmental alerts suggest that avoidance behavior becomes increasingly significant across all age groups as restrictions become more severe.

Susceptible windows of prenatal and postnatal fine particulate matter exposures and attention-deficit hyperactivity disorder symptoms in early childhood

Few prior studies have explored windows of susceptibility to fine particulate matter (PM2.5) in both the prenatal and postnatal periods and children's attention-deficit/hyperactivity disorder (ADHD) symptoms.We analyzed data from 1416 mother-child pairs from the Spanish INMA (INfancia y Medio Ambiente) Study (2003–2008). Around 5 years of age, teachers reported the number of ADHD symptoms (i.e., inattention, hyperactivity/impulsivity) using the ADHD Diagnostic and Statistical Manual of Mental Disorders. Around 7 years of age, parents completed the Conners' Parent Rating Scales, from which we evaluated the ADHD index, cognitive problems/inattention, hyperactivity, and oppositional subscales, reported as age- and sex-standardized T-scores. Daily residential PM2.5 exposures were estimated using a two-stage random forest model with temporal back-extrapolation and averaged over 1-week periods in the prenatal period and 4-week periods in the postnatal period. We applied distributed lag non-linear models within the Bayesian hierarchical model framework to identify susceptible windows of prenatal or postnatal exposure to PM2.5 (per 5-μg/m3) for ADHD symptoms. Models were adjusted for relevant covariates, and cumulative effects were reported by aggregating risk ratios (RRcum) or effect estimates (βcum) across adjacent susceptible windows.A similar susceptible period of exposure to PM2.5 (1.2–2.9 and 0.9–2.7 years of age, respectively) was identified for hyperactivity/impulsivity symptoms assessed ~5 years (RRcum = 2.72, 95% credible interval [CrI] = 1.98, 3.74) and increased hyperactivity subscale ~7 years (βcum = 3.70, 95% CrI = 2.36, 5.03). We observed a susceptibility period to PM2.5 on risk of hyperactivity/impulsivity symptoms ~5 years in gestational weeks 16–22 (RRcum = 1.36, 95% CrI = 1.22, 1.52). No associations between PM2.5 exposure and other ADHD symptoms were observed.We report consistent evidence of toddlerhood as a susceptible window of PM2.5 exposure for hyperactivity in young children. Although mid-pregnancy was identified as a susceptible period of exposure on hyperactivity symptoms in preschool-aged children, this association was not observed at the time children were school-aged.

Fine Particulate Matter Exposure and Health Impacts from Indoor Activities

Exposure to fine particulate matter (PM2.5) is an important contributor to global human disease burden, particularly indoors where people spend the majority of their time and exposure is highest. We propose a framework linking indoor PM2.5 emissions from human activities to exposure and health impacts, expressed in Disability-Adjusted Life Years (DALY). Derived dynamic indoor PM2.5 concentrations—capturing temporal variations through different window-opening scenarios and air renewal rates—are used to estimate uncertainty for a parametric model (up to a factor of 114). Intake fractions (fraction of emitted substance taken in (μgintake/μgemitted)), effect factors (μDALY/μgintake), related impact characterisation factors (health impact per unit mass emitted (μDALY/μgemitted)), and impact scores (health impact per hour activity (μDALY/hactivity)) are provided for 19 one-hour indoor activities and can be flexibly scaled to real activity durations. Indoor concentrations exceeded recommended World Health Organization (WHO) limits for all activities at low ventilation rates. Per person, 98 to 119 μDALY/hactivity (52 to 63 minuteslost/hactivity) was associated with traditional fuel cook stoves, with high air renewal rates (3 and 14 h-1). The burning of candles, at low air renewal rates of 0.2 to 0.6 h-1, results in 7 to 11 μDALY/hactivity (4 to 11 minuteslost/hactivity). Derived impact scores and characterisation factors serve as a starting point for integrating indoor PM2.5 emissions and exposure into life cycle impact and public health assessments.

Exploring Regional Reduction Pathways for Human Exposure to Fine Particulate Matter (PM2.5) Using a Traffic Assignment Model.

An exposure-based traffic assignment (TA) model is used to quantify primary and secondary fine particulate matter (PM2.5) exposure from on-road vehicle flow on the Chicago Metropolitan Area regional network. PM2.5 exposure due to emissions from light-duty vehicles, heavy-duty trucks, public transportation, and electricity generation for electric vehicle charging and light-rail transportation is considered. The model uses travel demand data disaggregated by time-of-day period and vehicle user class to compare the exposure impacts of two TA optimization scenarios: a baseline user equilibrium with respect to travel time (UET) and a system optimal with respect to pollutant intake (SOI). Estimated baseline PM2.5 exposure damages are $3.7B-$8.3B/year. The SOI uses exposure-based vehicle rerouting to reduce total damages by 8.2%, with high-impacted populations benefiting from 10% to 20% reductions. However, the SOI's rerouting principle leads to a 66% increase in travel time. The model is then used to quantify the mitigation potential of different exposure reduction strategies, including a bi-objective optimization formulation that minimizes travel time and PM2.5 exposure concurrently, adoption of a cleaner vehicle fleet, higher public transportation use, particle filtration, and exposure-based truck routing. Exposure reductions range between 1% and 40%, but collective adoption of all strategies would lead to reductions upward of 50%.

Effects of personal exposure to the oxidative potential of PM2.5 on oxidative stress biomarkers in pregnant women

Oxidative stress is a prominent pathway for the health effects associated with fine particulate matter (PM2.5) exposure. Oxidative potential (OP) of PM has been associated to several health endpoints, but studies on its impact on biomarkers of oxidative stress remains insufficient. 300 pregnant women from the SEPAGES cohort (France) carried personal PM2.5 samplers for a week and OP was measured using ascorbic acid (AA) and dithiothreitol (DTT) assays, and normalized by 1) PM2.5 mass (OPm) and 2) sampled air volume (OPv). A pool of three urine spots collected on the 7th day of PM sampling was analyzed for biomarkers, namely 8-hydroxy-2-deoxyguanosine (8-OHdG), malondialdehyde (MDA) and 8-isoprostaglandin-F2α (8-isoPGF2α). Associations were investigated using adjusted multiple linear regressions. OP effects were additionally investigated by stratifying by median PM2.5 concentration (14 μg m−3). In the main models, no association was observed with 8-isoPGF2α, nor MDA. An interquartile range (IQR) increase in OPmAA exposure was associated with increased 8-OHdG (percent change: 6.2 %; 95 % CI: 0.2 % to 12.6 %). In the stratified analysis, exposure to OPmAA was associated with 8-OHdG for participants exposed to low levels of PM2.5 (percent change: 11.4 %; 95 % CI: 3.3 % to 20.1 %), but not for those exposed to high levels (percent change: −1.0 %; 95 % CI: −10.6 % to 9.6 %). Associations for OPmDTT also followed a similar pattern (p-values for OPmAA-PM and OPmDTT-PM interaction terms were 0.12 and 0.11, respectively). Overall, our findings suggest that OPmAA may be associated with increased DNA oxidative damage. This association was not observed with PM2.5 mass concentration exposure. The effects of OPmAA in 8-OHdG tended to be stronger at lower (below median) vs. higher concentrations of PM2.5. Further epidemiological, toxicological and aerosol research are needed to further investigate the OPmAA effects on 8-OHdG and the potential modifying effect of PM mass concentration on this association.

Cumulative effect of PM2.5 components is larger than the effect of PM2.5 mass on child health in India

While studies on ambient fine particulate matter (PM2.5) exposure effect on child health are available, the differential effects, if any, of exposure to PM2.5 species are unexplored in lower and middle-income countries. Using multiple logistic regression, we showed that for every 10 μg m−3 increase in PM2.5 exposure, anaemia, acute respiratory infection, and low birth weight prevalence increase by 10% (95% uncertainty interval, UI: 9–11), 11% (8–13), and 5% (4–6), respectively, among children in India. NO3-, elemental carbon, and NH4+ were more associated with the three health outcomes than other PM2.5 species. We found that the total PM2.5 mass as a surrogate marker for air pollution exposure could substantially underestimate the true composite impact of different components of PM2.5. Our findings provide key indigenous evidence to prioritize control strategies for reducing exposure to more toxic species for greater child health benefits in India.

Dynamic changes in ambient PM2.5 and body mass index among old adults: a nationwide cohort study.

Outdoor air pollution has been considered as a severe environmental health issue that almost affecting everyone in the world, and intensive actions were launched. However, little is known about the association between dynamic changes in ambient fine particulate matter (PM2.5) exposure and body mass index (BMI) among old adults. To investigate the dynamic changes in ambient PM2.5 and body mass index among the elderly, we included a total of 7204 participants from 28 provinces of China during 2011-2015 in the China Health and Retirement Longitudinal Study (CHARLS). Ambient fine particle matter (PM2.5) was estimated using a well-validated space-time extremely randomized trees model. Change in PM2.5 and BMI (ΔPM2.5 and ΔBMI) were calculated as the value at a follow-up visit minus value at baseline. Linear mixed-effects models were applied to quantify the associations, controlling for sociodemographic factors. We found that per 1 μg/m3 increase in PM2.5 exposure was associated with a 0.031-0.044 kg/m2 increase in BMI among the elderly. We observed an approximate linear concentration-response relationship of PM2.5 and BMI in each visit. Each 1 μg/m3 increase in ΔPM2.5 exposure was associated with an increase in ΔBMI (β = 0.040, 95% CI 0.030, 0.049), while per 1 μg/m3 decrease in the ΔPM2.5 exposure level was associated with a decrease in ΔBMI (β = -0.016, 95% CI -0.027, -0.004). Our findings suggest that dynamic changes in ambient PM2.5 was positively associated with changes in BMI among old Chinese population.

Studying the economic burden of premature mortality related to PM2.5 and O3 exposure in Greece between 2004 and 2019

The detrimental direct effects of air pollution on public health have been well-determined; however, of relevant importance are also the indirect effects on the economy. Based on the value of statistical life (VSLs) and the willingness to pay (WTP) method, we estimated the economic cost resulting from premature mortality associated with fine particulate matter (PM2.5) and ground-level ozone (O3) exposure across Greece during 2004–2019, under a constant and a changing income elasticity scenario. The spatiotemporal trends of the economic burden were also investigated. The total economic burden attributable to premature mortality due to exposure to PM2.5 and O3 for the 16-year period was estimated at € 66.34 billion under the constant scenario and at € 273.65 billion under the changing scenario. A dramatic decline of the mortality cost was observed from 2009 to 2019 in the changing scenario, reflecting various socio-economic factors and income losses, as opposed to a less profound downward trend under the constant scenario, where the annual Gross Domestic Product (GDP) and Consumer Price Index (CPI) variances were not taken into account. During the study period, PM2.5 contributed the most to the economic loss, while the contribution of O3 was much less. The spatiotemporal patterns observed here may prove an effective means of communicating these trends to policy-makers and may feed the design of strategies for protecting public health and safeguarding the economic growth.

The burden of cardiovascular disease associated with PM2.5 exposure in the Portuguese population

Abstract Background Exposure to air pollution has been associated with increased mortality, premature mortality, and morbidity. A causal relationship between fine particulate matter (PM2.5) exposure and cardiovascular morbidity and mortality was demonstrated by the American Heart Association. In 2020, exposure to PM2.5 concentrations above limits defined by World Health Organization was responsible for 238,000 and 2,600 premature deaths in the European Union and in Portugal, respectively. Aim To estimate the impact on cardiovascular diseases (CVD) attributable to exposure to PM2.5 between 2010 and 2020, expressed as years of life lost (YLL), in Portugal. Methods National Statistics databases were used to collect the number of cardiovascular mortality cases between 2010 and 2020. The atmospheric levels of PM2.5 were obtained from Online Database on Air Quality of the Portuguese Environment Agency. When PM2.5 data were absent, PM10 data were used to estimate the PM2.5 concentration through the ratio: PM2.5/PM10=0,65. The burden of disease was estimated as YLL. The YLLs due to PM2.5-associated stroke and IHD in the Portuguese adult population, older than 30 years, were determined using the population-attributable fraction (PAF). Results YLLs per year for stroke and IHD were estimated as 41,489.60 (95% CI: 34,610.68 - 48,368.52) YLL and 27,573.44 (95% CI: 24,939.94 - 30,206.93) YLL respectively. Between 2010 and 2020, the crude number of YLL in mainland Portugal due to PM2.5 exposure-associated stroke and IHD decreased. The YLLs for IHD and for stroke are higher for men than for women. However, for stroke, the YLLs do not demonstrate as significant a difference as for IHD. Conclusions These findings provide evidence of the impact of air pollution on human health, which are crucial for decision-making. Acknowledgments This work is funded by FCT/MCTES through national funds to PMCardImpact (EXPL/SAU-PUB/0944/2021). Key messages • Exposure to PM2.5 has a significant health impact concerning cardiovascular mortality. • Estimating burden of disease contributes for the decision making and environmental policies.

Long-term association of air pollution and incidence of lung cancer among older Americans: A national study in the Medicare cohort

BackgroundDespite strong evidence of the association of fine particulate matter (PM2.5) exposure with an increased risk of lung cancer mortality, few studies had investigated associations of multiple pollutants simultaneously, or with incidence, or using causal methods. Disparities were also understudied. ObjectivesWe investigated long-term effects of PM2.5, nitrogen dioxide (NO2), warm-season ozone, and particle radioactivity (PR) exposures on lung cancer incidence in a nationwide cohort. MethodsWe conducted a cohort study with Medicare beneficiaries (aged ≥ 65 years) continuously enrolled in the fee-for-service program in the contiguous US from 2001 to 2016. Air pollution exposure was averaged across three years and assigned based on ZIP code of residence. We fitted Cox proportional hazards models to estimate the hazard ratio (HR) for lung cancer incidence, adjusted for individual- and neighborhood-level confounders. As a sensitivity analysis, we evaluated the causal relationships using inverse probability weights. We further assessed effect modifications by individual- and neighborhood-level covariates. ResultsWe identified 166,860 lung cancer cases of 12,429,951 studied beneficiaries. In the multi-pollutant model, PM2.5 and NO2 exposures were statistically significantly associated with increased lung cancer incidence, while PR was marginally significantly associated. Specifically, the HR was 1.008 (95% confidence interval [CI]: 1.005, 1.011) per 1-μg/m3 increase in PM2.5, 1.013 (95% CI: 1.012, 1.013) per 1-ppb increase in NO2, and 1.005 (0.999, 1.012) per 1-mBq/m3 increase in PR. At low exposure levels, all pollutants were associated with increased lung cancer incidence. Men, older individuals, Blacks, and residents of low-income neighborhoods experienced larger effects of PM2.5 and PR. DiscussionLong-term PM2.5, NO2, and PR exposures were independently associated with increased lung cancer incidence among the national elderly population. Low-exposure analysis indicated that current national standards for PM2.5 and NO2 were not restrictive enough to protect public health, underscoring the need for more stringent air quality regulations.

PM2.5-attributable mortality burden variability in the continental U.S.

Epidemiologic studies have consistently observed associations between fine particulate matter (PM2.5) exposure and premature mortality. These studies use air quality concentration information from a combination of sources to estimate pollutant exposures and then assess how mortality varies as a result of differing exposures. Health impact assessments then typically use a single log-linear hazard ratio (HR) per health outcome to estimate counts of avoided human health effects resulting from air quality improvements. This paper estimates the total PM2.5-attributable premature mortality burden using a variety of methods for estimating exposures and quantifying PM2.5-attributable deaths in 2011 and 2028. We use: 1) several exposure models that apply a wide range of methods, and 2) a variety of HRs from the epidemiologic literature that relate long-term PM2.5 exposures to mortality among the U.S. population. We then further evaluate the variability of aggregated national premature mortality estimates to stratification by race and/or ethnicity or exposure level (e.g., below the current annual PM2.5 National Ambient Air Quality Standards). We find that unstratified annual adult mortality burden incidence estimates vary more (e.g., ∼3-fold) by HR than by exposure model (e.g., <10%). In addition, future mortality burden estimates stratified by race/ethnicity are larger than the unstratified estimates of the entire population, and studies that stratify PM2.5-attributable mortality HRs by an exposure concentration threshold led to substantially higher estimates. These results are intended to provide transparency regarding the sensitivity of mortality estimates to upstream input choices.

Gestational exposure to ambient fine particulate matter disrupts maternal hepatic lipid metabolism

Pregnancy is a unique physiological stage for females as well as a vulnerable period for pollutant exposure. The effect of gestational ambient fine particulate matter (PM2.5) exposure on maternal lipid metabolism during pregnancy is rarely observed, and the mechanism is unknown. In the current study, pregnant C57BL/6 mice were randomly assigned to either ambient PM2.5 or filtered air exposure chambers since gestational day (GD) 0. Meanwhile, non-pregnant female mice were housed as controls in each exposure chamber. PM2.5 exposure exerted no significant effect on body weight gain or the body composition during pregnancy. Pregnant mice exposed to PM2.5 demonstrated improved glucose tolerance, whereas non-pregnant mice showed an increased fasting blood glucose level after PM2.5 exposure with no alterations in glucose tolerance. PM2.5 exposure exerted no significant effect on total lipid content in serum during pregnancy, while an increased serum total lipid level was found in non-pregnant mice exposed to PM2.5. PM2.5 exposure had no effect on total liver lipid levels, it increased several triacylglycerol (TAG) species and total cholesterol esters (CEs) in pregnant mice but lowered a considerable amount in non-pregnant mice’ livers. Furthermore, gestational exposure to PM2.5 enhanced the expression of key enzymes in fatty acid uptake, de novo lipid synthesis, and β oxidation, and inhibited molecules for lipid export in mice liver. Conversely, PM2.5 exposure upregulated proteins involved in hepatic lipolysis and lipid export in non-pregnant mice. These results suggest that the interference of PM2.5 exposure during pregnancy on the lipid metabolism, particularly the hepatic lipid metabolism, differs from that during non-pregnancy. This study provides toxicological evidence that PM2.5 exposure during pregnancy disrupts the lipid metabolism of the liver and provides a basis for protecting vulnerable populations.

Mediating effect of body fat percentage in the association between ambient particulate matter exposure and hypertension: a subset analysis of China hypertension survey

BackgroundHypertension caused by air pollution exposure is a growing concern in China. The association between air pollutant exposure and hypertension has been found to be potentiated by obesity, however, little is known about the processes mediating this association. This study investigated the association between fine particulate matter (aerodynamic equivalent diameter ≤ 2.5 microns, PM2.5) exposure and the prevalence of hypertension in a representative population in southern China and tested whether obesity mediated this association.MethodsA total of 14,308 adults from 48 communities/villages in southern China were selected from January 2015 to December 2015 using a stratified multistage random sampling method. Hourly PM2.5 measurements were collected from the China National Environmental Monitoring Centre. Restricted cubic splines were used to analyze the nonlinear dose-response relationship between PM2.5 exposure and hypertension risk. The mediating effect mechanism of obesity on PM2.5-associated hypertension was tested in a causal inference framework following the approach proposed by Imai and Keele.ResultsA total of 20.7% (2966/14,308) of participants in the present study were diagnosed with hypertension. Nonlinear exposure-response analysis revealed that exposure to an annual mean PM2.5 concentration above 41.8 µg/m3 was associated with increased hypertension risk at an incremental gradient. 9.1% of the hypertension burden could be attributed to exposure to elevated annual average concentrations of PM2.5. It is noteworthy that an increased body fat percentage positively mediated 59.3% of the association between PM2.5 exposure and hypertension risk, whereas body mass index mediated 34.3% of this association.ConclusionsThis study suggests that a significant portion of the estimated effect of exposure to PM2.5 on the risk of hypertension appears to be attributed to its effect on alterations in body composition and the development of obesity. These findings could inform intersectoral actions in future studies to protect populations with excessive fine particle exposure from developing hypertension.