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Abstract Background Air pollution has been associated with metabolic disease and obesity. Adipokines are potential mediators of these effects, but studies of air pollution-adipokine relationships are inconclusive. Macrophage and T cells in adipose tissue (AT) and blood modulate inflammation; however, the role of immune cells in air pollution-induced dysregulation of adipokines has not been studied. We examined the association between air pollution exposure and circulating and AT adipokine concentrations, and whether these relationships were modified by macrophage and T cell numbers in the blood and AT. Methods Fasting blood and abdominal subcutaneous AT biopsies were collected from 30 overweight/obese 18–26 year-old volunteers. Flow cytometry was used to quantify T effector (Teff, inflammatory) and regulatory (Treg, anti-inflammatory) lymphocytes and M1 [inflammatory] and M2 [anti-inflammatory]) macrophage cell number. Serum and AT leptin and adiponectin were measured using enzyme-linked immunosorbent assay (ELISA). Exposure to near-roadway air pollution (NRAP) from freeway and non-freeway vehicular sources and to regional particulate matter, nitrogen dioxide and ozone were estimated for the year prior to biopsy, based on participants’ residential addresses. Linear regression models were used to examine the association between air pollution exposures and adipokines and to evaluate effect modification by immune cell counts. Results An interquartile increase in non-freeway NRAP exposure during 1 year prior to biopsy was associated with higher leptin levels in both serum [31.7% (95% CI: 10.4, 52.9%)] and AT [19.4% (2.2, 36.6%)]. Non-freeway NRAP exposure effect estimates were greater among participants with greater than median Teff/Treg ratio and M1/M2 ratio in blood, and with greater M1 counts in AT. No adipokine associations with regional air pollutants were found. Discussion Our results suggest that NRAP may increase serum leptin levels in obese young adults, and this association may be promoted in a pro-inflammatory immune cell environment in blood and AT.

Background: Air pollution has been associated with metabolic disease and obesity. Adipokines are potential mediators of these effects, but studies of air pollution-adipokine relationships are inconclusive. Macrophage and T cells in adipose tissue (AT) and blood modulate inflammation; however, the role of immune cells in air pollution-induced dysregulation of adipokines has not been studied. We examined the association between air pollution exposure and circulating and AT adipokine concentrations, and whether these relationships were modified by macrophage and T cell numbers in the blood and AT.Methods: Fasting blood and abdominal subcutaneous AT biopsies were collected from 30 overweight/obese 18-26 year-old volunteers. Flow cytometry was used to quantify T effector (Teff, inflammatory) and regulatory (Treg, anti-inflammatory) lymphocytes and M1 [inflammatory] and M2 [anti-inflammatory]) macrophage cell number. Serum and AT leptin and adiponectin were measured using enzyme-linked immunosorbent assay (ELISA). Exposure to near-roadway air pollution (NRAP) from freeway and non-freeway vehicular sources and to regional particulate matter, nitrogen dioxide and ozone were estimated for the year prior to biopsy, based on participants' residential addresses. Linear regression models were used to examine the association between air pollution exposures and adipokines and to evaluate effect modification by immune cell counts.Results: An interquartile increase in non-freeway NRAP exposure during 1 year prior to biopsy was associated with higher leptin levels in both serum [31.7% (95% CI: 10.4, 52.9%)] and AT [19.4% (2.2, 36.6%)]. Non-freeway NRAP exposure effect estimates were greater among participants with greater than median Teff/Treg ratio and M1/M2 ratio in blood, and with greater M1 counts in AT. No adipokine associations with regional air pollutants were found.Discussion: Our results suggest that NRAP may increase serum leptin levels in obese young adults, and this association may be promoted in a pro-inflammatory immune cell environment in blood and AT. [ABSTRACT FROM AUTHOR]

Exposure to ambient and near-roadway air pollution during pregnancy has been linked with several adverse health outcomes for pregnant women and their babies. Emerging research indicates that microRNA (miRNA) expression can be altered by exposure to air pollutants in a variety of tissues. Additionally, miRNAs from breast tissue and circulating miRNAs have previously been proposed as a biomarker for breast cancer diagnosis and prognosis. Therefore, this study sought to evaluate the associations between pregnancy exposures to ambient (PM _10 , PM _2.5 , NO _2 , O _3 ) and near-roadway air pollution (total NO _x , freeway NO _x , non-freeway NO _x ) with breast milk extracellular vesicle miRNA (EV-miRNA), measured at 1-month postpartum, in a cohort of 108 Latina women living in Southern California. We found that PM _10 exposure during pregnancy was positively associated with hsa-miR-200c-3p, hsa-miR-200b-3p, and hsa-let-7c-5p, and was negatively associated with hsa-miR-378d. We also found that pregnancy PM _2.5 exposure was positively associated with hsa-miR-200c-3p and hsa-miR-200b-3p. First and second trimester exposure to PM _10 and PM _2.5 was associated with several EV-miRNAs with putative messenger RNA targets related to cancer. This study provides preliminary evidence that air pollution exposure during pregnancy is associated with human milk EV-miRNA expression.

Abstract Background Evidence suggests that childhood near-roadway air pollution (NRAP) exposures contribute to increased body mass index (BMI); however, effects of NRAP exposure during the vulnerable periods including in utero and first year of life have yet to be established. In this study, we examined whether exposure to elevated concentrations of NRAP during in utero and/or first year of life increase childhood BMI growth. Methods Participants in the Children’s Health Study enrolled from 2002 to 2003 with annual visits over a four-year period and who changed residences before study entry were included (n = 2318). Annual height and weight were measured and lifetime residential NRAP exposures including in utero and first year of life periods were estimated by nitrogen oxides (NOx) using the California line-source dispersion model. Linear mixed effects models assessed in utero or first year near-road freeway and non-freeway NOx exposures and BMI growth after adjusting for age, sex, race/ethnicity, parental education, Spanish questionnaire, and later childhood near-road NOx exposure. Results A two-standard deviation difference in first year of life near-road freeway NOx exposure was associated with a 0.1 kg/m2 (95% confidence interval (CI): 0.03, 0.2) faster increase in BMI growth per year and a 0.5 kg/m2 (95% CI: 0.02, 0.9) higher attained BMI at age 10 years. Conclusions Higher exposure to early life NRAP increased the rate of change of childhood BMI and resulted in a higher attained BMI at age 10 years that were independent of later childhood exposures. These findings suggest that elevated early life NRAP exposures contribute to increased obesity risk in children.

Highlights • Air pollution from motor vehicles is harmful to human health. • Study analyzes municipal zoning and zoning changes near major roadways in Los Angeles. • Municipal zoning permits residential development on 92% of parcels within 500 feet of a freeway. • Los Angeles disproportionately enables multifamily housing, rather than single-family housing, near major roadways. Abstract Air pollution from motor vehicles harms the health of those who live near freeways and other high-traffic roads. Land use regulations may permit, prohibit, or impose special conditions on housing near major roadways. This paper answers two questions: First, how is residential development near major roadways regulated? Second, how common are zoning changes near major roadways, and what factors explain these changes? This paper compares the zoning designations of near-roadway parcels with others in the city, and uses two sets of logistic regression models to analyze near-roadway zoning. The results show that residential development is permitted on most near-roadway parcels, including more than 92% of those within 500 feet of a freeway. One of the main explanations is that Los Angeles’s hierarchical zoning structure allows housing development in most commercial zones. While many of these parcels have commercial development today, they could be redeveloped for residential uses in the future. Larger shares of near-roadway parcels were upzoned to allow higher residential densities compared with parcels elsewhere in the city, but this difference is explained by other locational factors. [ABSTRACT FROM AUTHOR]

Growing evidence indicates exposure to air pollution contributes to obesity and cardiometabolic disease risk in children and adults, however studies are lacking in young adulthood, an important transitional period in the life course. The aim of this study was to examine the associations of short- and long-term regional ambient and near-roadway air pollution (NRAP) exposures on adiposity and cardiometabolic health in young adults aged 17–22 years. From 2014 to 2018, a subset of participants (n = 158) were recruited from the Children's Health Study to participate in the Meta-AIR (Metabolic and Asthma Incidence Research) study to assess obesity (body composition and abdominal adiposity) and cardiometabolic health (fasting glucose, fasting insulin and lipid profiles) measures. Prior 1-month and 1-year average air pollution exposures were calculated from residential addresses. This included nitrogen dioxide (NO 2), ozone (O 3), particulate matter with aerodynamic diameter < 10 μm (PM 10), particulate matter with aerodynamic diameter < 2.5 μm (PM 2.5) and NRAP (freeway, non-freeway, and total nitrogen oxides (NO x)) exposures. Linear regression models examined associations of prior 1-month (short-term) and 1-year (long-term) air pollution exposures on obesity and cardiometabolic factors adjusting for covariates and past childhood air pollution exposures. In the Meta-AIR study, we conducted a comprehensive analysis with short- and long-term regional ambient and NRAP exposures (in both single- and multi-pollutant models) and obesity- and cardiometabolic-related outcomes and found associations with a few outcomes. A 1 standard deviation (SD) change in long-term NO 2 exposure was associated with a 11.3 mg/dL higher level of total cholesterol (p = 0.04) and 9.4 mg/dL higher level of low-density lipoproteins (LDL)-cholesterol (p = 0.04). Amongst obese participants, associations between long-term NO 2 and total cholesterol and LDL-cholesterol were 4.5 and 9 times larger than the associations in non-obese participants (p interaction = 0.008 and 0.03, respectively). Additionally, we observed a statistically significant association with increased short-term O 3 exposure and higher triglyceride and very-low-density lipoprotein (VLDL) cholesterol levels (p = 0.04), lower high-density lipoprotein (HDL) cholesterol levels (p = 0.03), and higher hepatic fat levels (p = 0.02). Amongst glucose-related factors, long-term PM 2.5 exposure was associated with higher levels of insulin area under the curve (p = 0.03). There were no other statistically significant associations with short- or long-term air pollutants and BMI, other measures of adiposity, and cardiometabolic outcomes. Higher exposure to regional air pollutants, namely prior 1-year average NO 2 , was associated with higher fasting serum lipid measures. These associations were more pronounced in obese participants, suggesting obesity may exacerbate the effects of air pollution exposure on lipid levels in young adults. This study did not find any other associations between short- and long-term ambient and NRAP exposures across a range of other obesity and cardiometabolic indicators. Further studies in young adults are warranted as our study suggests potential deleterious associations of both short- and long-term air pollution exposures and lipid metabolism. • We assessed measures of adiposity, cardiometabolic health in 158 young adults. • Ambient air pollution was associated with some cardiometabolic risk factors. • Long-term NO 2 was associated higher total cholesterol and LDL-C levels. • Associations between NO 2 and lipids were more pronounced in obese participants. • Short-term O 3 was associated with higher triglycerides and VLDL-C and lower HDL-C. [ABSTRACT FROM AUTHOR]

Background: Evidence suggests that childhood near-roadway air pollution (NRAP) exposures contribute to increased body mass index (BMI); however, effects of NRAP exposure during the vulnerable periods including in utero and first year of life have yet to be established. In this study, we examined whether exposure to elevated concentrations of NRAP during in utero and/or first year of life increase childhood BMI growth.Methods: Participants in the Children's Health Study enrolled from 2002 to 2003 with annual visits over a four-year period and who changed residences before study entry were included (n = 2318). Annual height and weight were measured and lifetime residential NRAP exposures including in utero and first year of life periods were estimated by nitrogen oxides (NOx) using the California line-source dispersion model. Linear mixed effects models assessed in utero or first year near-road freeway and non-freeway NOx exposures and BMI growth after adjusting for age, sex, race/ethnicity, parental education, Spanish questionnaire, and later childhood near-road NOx exposure.Results: A two-standard deviation difference in first year of life near-road freeway NOx exposure was associated with a 0.1 kg/m2 (95% confidence interval (CI): 0.03, 0.2) faster increase in BMI growth per year and a 0.5 kg/m2 (95% CI: 0.02, 0.9) higher attained BMI at age 10 years.Conclusions: Higher exposure to early life NRAP increased the rate of change of childhood BMI and resulted in a higher attained BMI at age 10 years that were independent of later childhood exposures. These findings suggest that elevated early life NRAP exposures contribute to increased obesity risk in children. [ABSTRACT FROM AUTHOR]