Impact Of Particulate Matter Exposure Research Articles

Autophagy alleviates hippocampal neuroinflammation by inhibiting the NLRP3 inflammasome in a juvenile rat model exposed particulate matter

Ambient fine particulate matter (PM) is a global public and environmental problem. PM is closely associated with several neurological diseases, which typically involve neuroinflammation. We investigated the impact of PM exposure on neuroinflammation using both in vivo (in a juvenile rat model with PM exposure concentrations of 1, 2, and 10 mg/kg for 28 days) and in vitro (in BV-2 and HT-22 cell models with PM concentrations of 50–200 μg/ml for 24 h). We observed that PM exposure induced the activation of the NLRP3 inflammasome, leading to the production of IL-1β and IL-18 in the rat hippocampus and BV-2 cells. Furthermore, inhibition of the NLRP3 inflammasome with MCC950 effectively reduced neuroinflammation and ameliorated hippocampal damage. In addition, autophagy activation was observed in the hippocampus of PM-exposed rats, and the promotion of autophagy by rapamycin (Rapa) effectively attenuated the NLRP3-mediated neuroinflammation induced by PM exposure. However, autophagic flow was blocked in BV-2 cells exposed to PM, and Rapa failed to ameliorate NLRP3 inflammasome activation. We found that autophagy was activated in HT-22 cells exposed to PM and that treatment with Rapa reduced the release of reactive oxygen species (ROS) and malondialdehyde (MDA), as well as cell apoptosis. In a subsequent coculture model of BV-2 and HT-22 cells, we observed the activation of the NLRP3 inflammasome in BV-2 cells when the HT-22 cells were exposed to PM, and this activation was alleviated when PM-exposed HT-22 cells were pretreated with Rapa. Overall, our study revealed that PM exposure triggered hippocampal neuroinflammation by activating the NLRP3 inflammasome. Notably, autophagy mitigated NLRP3 inflammasome activation, potentially by reducing neuronal ROS and apoptosis. This research emphasized the importance of reducing PM exposure and provided valuable insight into its neurotoxicity.

Impact of Particulate Matter Exposure and Aerobic Exercise on Circulating Biomarkers of Oxidative Stress, Antioxidant Status, and Inflammation in Young and Aged Mice.

Exposure to particulate matter (PM) and exercise training can have antagonistic effects on inflammatory responses and the balance between pro-oxidants and antioxidants in the body. However, the underlying mechanisms of these effects remain unclear. This study aimed to investigate the effects of PM exposure and aerobic exercise training on oxidative stress, antioxidant status, and inflammation in mice of different ages. Two groups of male C57BL/6 mice, comprising forty 1-month-old and forty 12-month-old mice, were exposed to either PM or exercise training or both for 8 weeks. PM exposure led to significantly higher 8-hydroxydeoxyguanosine (8-OHdG), malondialdehyde (MDA), interleukin-1β (IL-1β), interleukin-6 (IL-6), and tumor necrosis factor α (TNF-α) levels (p < 0.05) and significantly lower superoxide dismutase (SOD) and catalase (CAT) activities (p < 0.05) in both age groups exposed to PM compared to the control groups. Conversely, aerobic exercise training led to significantly lower 8-OHdG, MDA, IL-1β, IL-6, and TNF-α levels (p < 0.05) and significantly higher SOD and CAT activities (p < 0.05) in both age groups receiving exercise training, compared to those exposed to PM. Moreover, young mice in the exercise training and PM group showed significantly lower 8-OHdG, MDA, and IL-1β levels (p < 0.05) and significantly higher SOD and CAT activities (p < 0.05) than young mice in the PM exposure group. However, these levels did not vary significantly between the group of old mice that either received exercise training or exposure to PM. Our results suggest that while PM exposure could cause pro-oxidant/antioxidant imbalances and inflammatory responses, regular aerobic exercise could ameliorate these negative effects, although these vary with age. Nevertheless, the antioxidant and anti-inflammatory effects of exercise were countered by PM exposure, especially in older mice.

Simulating the impact of particulate matter exposure on health-related behaviour: A comparative study of stochastic modelling and personal monitoring data.

Epidemiological and exposure studies concerning particulate matter (PM) often rely on data from sparse governmental stations. While low-cost personal monitors have some drawbacks, recent developments have shown that they can provide fairly accurate and fit-for-purpose data. Comparing a stochastic, i.e., agent-based model (ABM), with environmental, biometric and activity data, collected with personal monitors, could provide insight into how the two approaches assess PM exposure and dose. An ABM was constructed, simulating a PM exposure/dose assessment of 100 agents. Their actions were governed by inherent probabilities of performing an activity, based on population data. Each activity was associated with an intensity level, and a PM pollution level. The ABM results were compared with real-world results. Both approaches had comparable results, showing similar trends and a mean dose. Discrepancies were seen in the activities with the highest mean dose values. A stochastic model, based on population data, does not capture well some specifics of a local population. Combined, personal sensors could provide input for calibration, and an ABM approach can help offset a low number of participants. Implementing a function of agents influencing others transport choice, increased the importance of cycling/walking in the overall dose estimate. Activists, agents with an increased transport influence, did not play an important role at low PM levels. As concentrations rose, higher shares of activists (and their influence) caused the dose to increase. Simulating a person's PM exposure/dose in different scenarios and activities in a virtual environment provides researchers and policymakers with a valuable tool.

Potential causal links between long-term ambient particulate matter exposure and cerebrovascular mortality: Insights from a large cohort in southern China

Cohort studies conducted in North America and Europe have linked cerebrovascular mortality to long-term exposure to particulate matter (PM). However, limited evidence from large cohorts in high-exposure areas and the traditional approach of association assessment may cause residual confounding issues. In this study, we aimed to investigate the causal links between cerebrovascular mortality and long-term exposure to PM2.5, PM10, and PM2.5-10 in an ongoing cohort study with 580,757 participants in southern China. Using satellite-based estimates of PM concentration at a 1-km2 spatial resolution, we assigned exposure levels to each participant and used the marginal structural Cox model to assess the association between PM exposure and cerebrovascular mortality while accounting for time-varying covariates. We also explored the potential modification effects of sociodemographic and behavioral factors on the PM-health associations. Adjusted hazard ratios (HR) for overall cerebrovascular mortality were 1.041 (95% confidence interval (CI): 1.034–1.049) and 1.032 (95% CI: 1.026–1.038) for each 1 μg/m3 increase in PM2.5, and PM10, respectively. Similar trends were observed in the mortality risk from stroke and ischemic stroke, with HRs ranging from 1.040 to 1.069 and 1.025 to 1.052, respectively, across 2 p.m. exposures. The impact of PM exposure was generally more apparent among women, participants with primary school diplomas and below, and the subgroup under low-exposure. Multiple sensitivity analyses confirmed the robustness of the results. In conclusion, this sizable prospective cohort study hypothesizes causal links between long-term PM exposure and cerebrovascular mortality, particularly among vulnerable participants, supporting the rationale for reducing PM concentration in China to reduce cerebrovascular mortality.

Systems level insights into the impact of airborne exposure on SARS-CoV-2 pathogenesis and COVID-19 outcome – A multi-omics big data study

Coronavirus disease 2019 (COVID-19) is a viral pandemic caused by severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) that led to more than 800,00 deaths and continues to be a major threat worldwide. The scientific community has been studying the risk factors associated with SARS-CoV-2 infection and pathogenesis. Recent studies highlight the possible contribution of atmospheric air pollution, specifically particulate matter (PM) exposure as a co-factor in COVID-19 severity. Hence, meaningful translation of suitable omics datasets of SARS-CoV-2 infection and PM exposure is warranted to understand the possible involvement of airborne exposome on COVID-19 outcome. Publicly available transcriptomic data (microarray and RNA-Seq) related to COVID-19 lung biopsy, SARS-CoV-2 infection in epithelial cells and PM exposure (lung tissue, epithelial and endothelial cells) were obtained in addition with proteome and interactome datasets. System-wide pathway/network analysis was done through appropriate software tools and data resources. The primary findings are; 1. There is no robust difference in the expression of SARS-CoV-2 entry factors upon particulate exposure, 2. The upstream pathways associated with upregulated genes during SARS-CoV-2 infection considerably overlap with that of PM exposure, 3. Similar pathways were differentially expressed during SARS-CoV-2 infection and PM exposure, 4. SARS-CoV-2 interacting host factors were predicted to be associated with the molecular impact of PM exposure and 5. Differentially expressed pathways during PM exposure may increase COVID-19 severity. Based on the observed molecular mechanisms (direct and indirect effects) the current study suggests that airborne PM exposure has to be considered as an additional co-factor in the outcome of COVID-19.

Predictive and Preventive Mucosal Communications in Particulate Matter Exposure-Linked Renal Distress.

Despite research into the epidemiological link between exposure to particulate matter (PM) and renal disorder, there is limited information available on the etiological complexity and molecular mechanisms. Among the early responsive tissues to PM exposure, the mucosal barrier of the airway and alimentary tract may be a crucial source of pathologic mediators leading to inflammatory renal diseases, including chronic kidney disease (CKD). Given that harmful responses and products in mucosa exposed to PM may enter the circulation and cause adverse outcomes in the kidney, the aim of the present review was to address the impact of PM exposure on the mucosal barrier and the vicious feedback cycle in the mucosal environment. In addition to the PM-induced alteration of mucosal barrier integrity, the microbial community has a pivotal role in the xenobiotic metabolism and individual susceptibility to PM toxicity. The dysbiosis-induced deleterious metabolites of PM and nutrients are introduced systemically via a disrupted mucosal barrier, contributing to renal injuries and pathologic severity. In contrast, the progress of mucosa-associated renal disease is counteracted by endogenous protective responses in the mucosa. Along with direct elimination of the toxic mediators, modulators of the mucosal microbial community should provide a promising platform for mucosa-based personalized interventions against renal disorders caused by air pollution.

In Utero Exposure to Particulate Air Pollution during Pregnancy: Impact on Birth Weight and Health through the Life Course.

In high-income countries, and increasingly in lower- and middle-income countries, chronic non-communicable diseases (NCDs) have become the primary health burden. It is possible that in utero exposure to environmental pollutants such as particulate matter (PM) may have an impact on health later in life, including the development of NCDs. Due to a lack of data on foetal growth, birth weight is often used in epidemiologic studies as a proxy to assess impacts on foetal development and adverse birth outcomes since it is commonly recorded at birth. There are no research studies with humans that directly link PM exposure in utero to birth weight (BW) and subsequently, the effects of lower BW on health outcomes in old age. It is, however, plausible that such associations exist, and it is thus important to assess the potential public health impacts of PM across the life course, and it is plausible to use birth weight as an indicator of risk. We therefore split this narrative review into two parts. In the first part, we evaluated the strength of the evidence on the impact of PM exposure during the entire pregnancy on birth weight outcomes in ten meta-analyses. In the second part, we reviewed the literature linking lower birth weight to childhood and adult chronic cardiovascular disease to explore the potential implications of PM exposure in utero on health later in life. Within the reviewed meta-studies on birth weight, there is sufficient evidence that PM pollution is associated with lower birth weight, i.e., the majority of meta-studies found statistically significant reductions in birth weight. From the second part of the review, it is evident that there is good evidence of associations between lower birth weight and subsequent cardiovascular disease risk. It is thus plausible that in utero exposure to PM is associated with lower birth weight and persisting biological changes that could be associated with adverse health effects in adulthood. Based on the reviewed evidence, however, the magnitude of later life cardiovascular health impacts from in utero exposure and its impact on BW are likely to be small compared to health effects from exposure to particulate air pollution over a whole lifetime.

Analysis of air pollution exposure in the area of Iasi county – a warning signal for lung health and the risk of developing COPD

Abstract Air pollution is a major threat to public health, and the effects of pollution are perceived in all countries of the world, by all social categories, regardless of age. Chronic obstructive pulmonary disease (COPD) has a growing prevalence worldwide and an increasing number of risk factors that exacerbate symptoms and accelerate disease progression. Exposure to air pollution is one of the less studied and less investigated risk factors for COPD. Depending on the size and chemical nature of the pollutant, it can overcome the defence mechanism of the respiratory system and enter the lung tissues, thus causing some respiratory diseases. The World Health Organisation (WHO) reports that six major air pollutants have been identified, namely particulate matter (PM), ground-level ozone, carbon monoxide, sulphur dioxide, nitrogen dioxide and lead. The severe impact of PM exposure is demonstrated by the link between exposure to high concentrations of PM and certain severe diseases such as silicosis, lung cancer, cardiovascular disease and COPD. In Iași County, Romania, air quality measurements are performed by six automatic air quality monitoring stations, and the data obtained are used to create annual reports and these are also available online. Due to the high concentrations of air pollutants, the city of Iași is one of the three topmost polluted cities in Romania. A future assessment on the impact of air pollution on the health of the inhabitants of these cities and the implementation of new methods to improve air quality is needed.

The impact of prenatal exposure to PM2.5 on childhood asthma and wheezing: a meta-analysis of observational studies.

With the accelerated pace of economic development and modernization, air pollution has become one of the most focused public health problems. However, the impact of particulate matter exposure during pregnancy on childhood asthma and wheezing remains controversial. We performed this meta-analysis to explore the relationship between prenatal exposure to PM2.5 and childhood asthma and wheezing. Candidate papers were searched on PubMed, Web of Science, Embase, and Cochrane Library before July 15, 2019. The main characteristics of the included studies were extracted, and the quality was evaluated by the Newcastle-Ottawa Scale (NOS). A sensitivity analysis was performed to assess the impact of individual studies on the combined effects. The Egger and Begg tests were conducted to examine the publication bias. Nine studies were included in the final analysis. Prenatal exposure to PM2.5 significantly increased the risk of childhood asthma and wheezing (OR = 1.06, 95% CI 1.02-1.11; per 5μg/m3). Maternal exposure was more strongly related to childhood asthma and wheezing before age 3 (OR = 1.15, 95% CI 1.00-1.31; per 5μg/m3) than after (OR = 1.04, 95% CI 1.00-1.09; per 5μg/m3). Children in developed countries showed more severe effects (OR = 1.14, 95% CI 1.02-1.27; per 5μg/m3). Children who were born to mothers with higher levels of prenatal exposure were at higher risk of asthma and wheezing (OR = 1.07, 95% CI 1.02-1.13; per 5μg/m3). This meta-analysis indicated that the impact of PM2.5 on childhood asthma and wheezing begins as early as utero, so regulating pollutant emission standards and strengthening prenatal protection are crucial to maternal and child health.

Impact of Particulate Matter Exposure and Surrounding "Greenness" on Chronic Absenteeism in Massachusetts Public Schools.

Chronic absenteeism is associated with poorer academic performance and higher attrition in kindergarten to 12th grade (K-12) schools. In prior research, students who were chronically absent generally had fewer employment opportunities and worse health after graduation. We examined the impact that environmental factors surrounding schools have on chronic absenteeism. We estimated the greenness (Normalized Difference Vegetation Index (NDVI)) and fine particulate matter air pollution (PM2.5) within 250 m and 1000 m respectively of each public school in Massachusetts during the 2012–2013 academic year using satellite-based data. We modeled chronic absenteeism rates in the same year as a function of PM2.5 and NDVI, controlling for race and household income. Among the 1772 public schools in Massachusetts, a 0.15 increase in NDVI during the academic year was associated with a 2.6% (p value < 0.0001) reduction in chronic absenteeism rates, and a 1 μg/m3 increase in PM2.5 during the academic year was associated with a 1.58% (p value < 0.0001) increase in chronic absenteeism rates. Based on these percentage changes in chronic absenteeism, a 0.15 increase in NDVI and 1 μg/m3 increase in PM2.5 correspond to 25,837 fewer students and 15,852 more students chronically absent each year in Massachusetts respectively. These environmental impacts on absenteeism reinforce the need to protect green spaces and reduce air pollution around schools.

Fine airborne particles: when alarming levels are the standard

ObjectivesTo quantify the contribution of each individual month to the annual mortality burden attributable to particulate matter (PM) in 2015 in Milan, Italy, after authorities and media considered December 2015 as an outlying month carrying an exceptional population exposure to PM. Study designWe used routinely available daily time series of air pollution and mortality to perform an assessment of the impact of PM exposure on population health. MethodsBy combining daily death counts with daily PM levels, as well as the yearly average of the number of deaths with the yearly average of PM concentrations, impact estimates were calculated in terms of deaths attributable (AD) to levels of PM10 and PM2.5 exceeding the daily or the annual European Union (EU) exposure limits. ResultsOn a monthly basis, the estimated AD for exceeding the daily EU limits for more than 35 days were 18.4 (PM10) and 33.2 (PM2.5) between January and March, and 20.0 and 31.9 between October and December, respectively. On an annual basis, the EU limit for PM10 was almost met and, therefore, the estimated impact in terms of AD was practically null. ConclusionsImpact results should be interpreted in the light of the skewness of the daily PM concentration distribution. The number of days above the limits is more important than the average annual concentration in determining the number of attributable deaths. The impact of PM on mortality is substantial during the whole winter season irrespective of its annual average concentration. Our estimates further stress the need for a revision of the current European air quality standards.

Exposure to inhaled atmospheric particulate matter enhances autoimmunity. (BA6P.125)

Abstract Epidemiological studies have demonstrated a relationship between exposure to atmospheric particulate matter (PM) and autoimmune disease. Multiple mechanisms have been proposed, including our research showing PM exposure in vitro can enhance Th17 differentiation in an aryl hydrocarbon receptor-dependent manner. The current study sought to determine the impact of PM exposure in vivo on immunity outside of the lung. In the 1st experiment, male B6 mice (n = 4 per group) were treated every 3 days with either vehicle or 800ug of SRM1949b, a representative sample of urban dust particles, in 20ul PBS i.n. for a total of 5 doses. One day after the last dose, splenocytes were cultured for 4 days with anti-CD3 and cytokines were measured. Treatment with PM increased IL-17A 3-fold but had no impact on IFNγ expression. In the 2nd experiment, female B6 mice (n = 4 per group) were treated every 3 days with vehicle or PM for a total of 9 doses. On the day of the 5th dose, a standard EAE protocol commenced. Clinical scoring using a 5-point scale began on d7 and ended on d21. All mice in both groups displayed EAE symptoms. Mice treated with PM had significantly higher mean peak score (3.5 + 0.3 vs 2.5 + 0.3 for PBS), trended toward having a higher mean clinical score and had earlier onset of disease. Together, these data suggest that inhaled PM exposure can impact immune responses beyond the lung, and support a mechanism where inhaled pollution aggravates autoimmunity.

PCV162 - The Short-Term Impact of Particulate Matter Exposure on the Risk of Prescription of Cardiorespiratory Drugs in Italy

PCV162 - The Short-Term Impact of Particulate Matter Exposure on the Risk of Prescription of Cardiorespiratory Drugs in Italy

A 12-week aerobic training program in an urban environment: effect on blood gene expression profiles and subclinical inflammatory markers

Background Exposure to particulate matter (PM) air pollution is known to contribute to inflammatory processes in humans. Aerobic exercise increases the ventilation rate, hence also the exposure to PM. Aims We investigated the impact of PM exposure during a 12-week aerobic training program on healthy volunteers by analyzing subclinical parameters at the start and at the end of the program. Methods One group (n=15) trained in an urban environment, whereas the second group (n=9) trained in a rural environment. Ultrafine Particle (UFP) concentrations were measured during each training session. Differential leukocyte counts, exhaled NO (eNO) and blood transcriptomics profiles were determined. Results Urban UFP concentrations were higher (p = 0.003) than in the rural environment. Leukocyte count (p = 0.022), neutrophil count (p = 0.04), and exhaled nitric oxide (p = 0.003) increased significantly in the urban group at the end of the program, and not in the rural group. A total of 816 genes were altered in expression (multiplicity corrected p-value&lt;0.05 and absolute fold change &gt; 1.5) in the urban group (399 upregulated genes, 417 downregulated genes), and 709 genes showed differential expression (665 upregulated genes, 44 downregulated genes) in the rural group. The expressions of 254 genes were altered in both groups. Gene Ontology analysis associated 55 genes to stress response. For example, an upregulation of interleukin 1 beta, superoxide dismutase and toll-like receptor 4 was observed in both groups. The analysis also revealed an interaction effect for 246 genes. Thirty nine genes were upregulated and two hundred and seven genes were downregulated when the urban group was compared to the rural group. This indicates that gene expression signals were changed depending on the location where the participants were exercising. Conclusions Our study has revealed that subclinical measurements and blood molecular patterns are significantly affected when healthy individuals exercising in an urban environment are compared to a rural environment.

Aerobic training in urban environment: blood gene expression profiling

Background Physical activity is a recommended life-style activity to promote health, while particulate matter (PM) exposure induces adverse health effects. The aim was to investigate the impact of PM exposure during aerobic training on the blood gene expression profile. Methods Healthy, untrained subjects participated in a 12-week aerobic training program (3 sessions/wk), one group (n=15) in an urban location, another group (n=9) in a rural location. Ultrafine particles (UFP) were measured at the training locations during the training sessions. Fitness levels (cooper-test) and whole-genome blood gene expression profiles in blood were determined before and after the program. The up or downregulation of the genes was called significant in case of a multiplicity corrected p-value&lt;0.05 and an effect size in terms of absolute fold change &gt; 1.5. Results UFP concentrations were higher (p = 0.003) in the urban location (7240 particles/cc) compared to the rural location (5621 particles/cc). Fitness level improved (p &lt; 0.0001) equally in both groups (p = 0.16).The expression of 816 genes was altered in the urban group (399 upregulated, 417 downregulated) and 709 genes showed differential expression (665 upregulated, 44 downregulated) in the rural group. The expression of 55 genes of the 254 genes that were altered in both groups were linked to stress response by Gene Ontology. One third of the differentially expressed genes was in common between the groups. The statistical analysis revealed an interaction effect for 246 genes. Thirty nine genes were upregulated and 207 genes were downregulated when the urban group was compared to the rural group. Gene Ontology analysis indicated a significant enrichment for the biological term cell death. No specific terms of genes were discovered that can be associated with immune or inflammatory processes. Conclusions Our study revealed a differential blood gene expression profile with aerobic training in an urban location compared to aerobic training in a rural location.

Airborne particulate matter selectively activates endoplasmic reticulum stress response in the lung and liver tissues

Recent studies have suggested a link between inhaled particulate matter (PM) exposure and increased mortality and morbidity associated with pulmonary and cardiovascular diseases. However, a precise understanding of the biological mechanism underlying PM-associated toxicity and pathogenesis remains elusive. Here, we investigated the impact of PM exposure in intracellular stress signaling pathways with animal models and cultured cells. Inhalation exposure of the mice to environmentally relevant fine particulate matter (aerodynamic diameter < 2.5 μm, PM(2.5)) induces endoplasmic reticulum (ER) stress and activation of unfolded protein response (UPR) in the lung and liver tissues as well as in the mouse macrophage cell line RAW264.7. Ambient PM(2.5) exposure activates double-strand RNA-activated protein kinase-like ER kinase (PERK), leading to phosphorylation of translation initiation factor eIF2α and induction of C/EBP homologous transcription factor CHOP/GADD153. Activation of PERK-mediated UPR pathway relies on the production of reactive oxygen species (ROS) and is critical for PM(2.5)-induced apoptosis. Furthermore, PM(2.5) exposure can activate ER stress sensor IRE1α, but it decreases the activity of IRE1α in splicing the mRNA encoding the UPR trans-activator X-box binding protein 1 (XBP1). Together, our study suggests that PM(2.5) exposure differentially activates the UPR branches, leading to ER stress-induced apoptosis through the PERK-eIF2α-CHOP UPR branch. This work provides novel insights into the cellular and molecular basis by which ambient PM(2.5) exposure elicits its cytotoxic effects that may be related to air pollution-associated pathogenesis.

Exposures to airborne particulate matter and adverse perinatal outcomes: a biologically plausible mechanistic framework for exploring potential

This article has three objectives: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review evidence showing that nutrition affects biologic pathways; and explain mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes. We propose an interdisciplinary framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework. The literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources. We present strategies for empirically testing the proposed model and developing future research efforts.

Exposures to Airborne Particulate Matter and Adverse Perinatal Outcomes: A Biologically Plausible Mechanistic Framework for Exploring Potential Effect Modification by Nutrition

ObjectivesThe specific objectives are threefold: to describe the biologically plausible mechanistic pathways by which exposure to particulate matter (PM) may lead to the adverse perinatal outcomes of low birth weight (LBW), intrauterine growth retardation (IUGR), and preterm delivery (PTD); review the evidence showing that nutrition affects the biologic pathways; and explain the mechanisms by which nutrition may modify the impact of PM exposure on perinatal outcomes.MethodsWe propose an interdisciplinary conceptual framework that brings together maternal and infant nutrition, air pollution exposure assessment, and cardiopulmonary and perinatal epidemiology. Five possible albeit not exclusive biologic mechanisms have been put forth in the emerging environmental sciences literature and provide corollaries for the proposed framework.ConclusionsProtecting the environmental health of mothers and infants remains a top global priority. The existing literature indicates that the effects of PM on LBW, PTD, and IUGR may manifest through the cardiovascular mechanisms of oxidative stress, inflammation, coagulation, endothelial function, and hemodynamic responses. PM exposure studies relating mechanistic pathways to perinatal outcomes should consider the likelihood that biologic responses and adverse birth outcomes may be derived from both PM and non-PM sources (e.g., nutrition). In the concluding section, we present strategies for empirically testing the proposed model and developing future research efforts.