Transportation Noise and Blood Pressure in a Population-Based Sample of Adults

Background: There is some evidence for an association between traffic noise and ischemic heart disease; however, associations with blood pressure have been inconsistent, and little is known about health effects of railway noise

Airborne Emissions from 1961 to 2004 of Benzo[a]pyrene from U.S. Vehicles per km of Travel Based on Tunnel Studies

We identified 13 historical measurements of polycyclic aromatic hydrocarbons (PAHs) in U.S. vehicular traffic tunnels that were either directly presented as tailpipe emission factors in μg per vehicle-kilometer or convertible to such a form. Tunnel measurements capture fleet cruise emissions. Emission factors for benzo[a]pyrene (BaP) for a tunnel fleet operating under cruise conditions were highest prior to the 1980s and fell from more than 30-μg per vehicle-km to approximately 2-μg/km in the 1990s, an approximately 15-fold decline. Total annual U.S. (cruise) emissions of BaP dropped by a lesser factor, because total annual km driven increased by a factor of 2.7 during the period. Other PAH compounds measured in tunnels over the 40-year period (e.g., benzo[ghi]perylene, coronene) showed comparable reduction factors in emissions. PAH declines were comparable to those measured in tunnels for carbon monoxide, volatile organic compounds, and particulate organic carbon. The historical PAH “source terms” determined from the data are relevant to quantifying the benefits of emissions control technology and can be used in epidemiological studies evaluating the health effects of exposure, such as those undertaken with breast cancer in New York State

Different genes interact with particulate matter and tobacco smoke exposure in affecting lung function decline in the general population

BACKGROUND: Oxidative stress related genes modify the effects of ambient air pollution or tobacco smoking on lung function decline. The impact of interactions might be substantial, but previous studies mostly focused on main effects of single genes. OBJECTIVES: We studied the interaction of both exposures with a broad set of oxidative-stress related candidate genes and pathways on lung function decline and contrasted interactions between exposures. METHODS: For 12679 single nucleotide polymorphisms (SNPs), change in forced expiratory volume in one second (FEV(1)), FEV(1) over forced vital capacity (FEV(1)/FVC), and mean forced expiratory flow between 25 and 75% of the FVC (FEF(25-75)) was regressed on interval exposure to particulate matter >10 microm in diameter (PM10) or packyears smoked (a), additive SNP effects (b), and interaction terms between (a) and (b) in 669 adults with GWAS data. Interaction p-values for 152 genes and 14 pathways were calculated by the adaptive rank truncation product (ARTP) method, and compared between exposures. Interaction effect sizes were contrasted for the strongest SNPs of nominally significant genes (p(interaction)>0.05). Replication was attempted for SNPs with MAF<10% in 3320 SAPALDIA participants without GWAS. RESULTS: On the SNP-level, rs2035268 in gene SNCA accelerated FEV(1)/FVC decline by 3.8% (p(interaction) = 2.5x10(-6)), and rs12190800 in PARK2 attenuated FEV1 decline by 95.1 ml p(interaction) = 9.7x10(-8)) over 11 years, while interacting with PM10. Genes and pathways nominally interacting with PM10 and packyears exposure differed substantially. Gene CRISP2 presented a significant interaction with PM10 (p(interaction) = 3.0x10(-4)) on FEV(1)/FVC decline. Pathway interactions were weak. Replications for the strongest SNPs in PARK2 and CRISP2 were not successful. CONCLUSIONS: Consistent with a stratified response to increasing oxidative stress, different genes and pathways potentially mediate PM10 and tobac smoke effects on lung function decline. Ignoring environmental exposures would miss these patterns, but achieving sufficient sample size and comparability across study samples is challengin

Adult lung function and long-term air pollution exposure. ESCAPE: a multicentre cohort study and meta-analysis.

The chronic impact of ambient air pollutants on lung function in adults is not fully understood. The objective of this study was to investigate the association of long-term exposure to ambient air pollution with lung function in adult participants from five cohorts in the European Study of Cohorts for Air Pollution Effects (ESCAPE). Residential exposure to nitrogen oxides (NO\u2082, NOx) and particulate matter (PM) was modelled and traffic indicators were assessed in a standardised manner. The spirometric parameters forced expiratory volume in 1 s (FEV\u2081) and forced vital capacity (FVC) from 7613 subjects were considered as outcomes. Cohort-specific results were combined using meta-analysis. We did not observe an association of air pollution with longitudinal change in lung function, but we observed that a 10 \u3bcg\ub7m(-3) increase in NO\u2082 exposure was associated with lower levels of FEV\u2081 (-14.0 mL, 95% CI -25.8 to -2.1) and FVC (-14.9 mL, 95% CI -28.7 to -1.1). An increase of 10 \u3bcg\ub7m(-3) in PM10, but not other PM metrics (PM2.5, coarse fraction of PM, PM absorbance), was associated with a lower level of FEV\u2081 (-44.6 mL, 95% CI -85.4 to -3.8) and FVC (-59.0 mL, 95% CI -112.3 to -5.6). The associations were particularly strong in obese persons. This study adds to the evidence for an adverse association of ambient air pollution with lung function in adults at very low levels in Europe

Long-term exposure to traffic-related PM(10) and decreased heart rate variability : is the association restricted to subjects taking ACE inhibitors?

BACKGROUND: Alterations in heart rate variability (HRV) are a potential link between exposure to traffic-related air pollution and cardiovascular mortality. OBJECTIVES: We investigated whether long-term exposure to traffic-related PM(10) (TPM(10)) is associated with HRV in older subjects and/or in participants taking specific cardiovascular treatment or with self-reported heart disease. METHODS: We included 1607 subjects from the general population aged 50 to 72years. These participants from the SAPALDIA cohort underwent ambulatory 24-hr electrocardiogram monitoring. Associations of average annual exposure to TPM(10) over 10years with HRV parameters from time and frequency domains were estimated using multivariable mixed linear models. Effect estimates are expressed as percent changes in geometric means. RESULTS: HRV was only associated with TPM(10) in participants under ACE inhibitor therapy (N=94). A 1mug/m(3) increment, approximately equivalent to an interquartile range, in 10year average TPM(10) was associated with decrements of 14.5% (95% confidence interval (CI), -25.9 to -1.3) in high frequency (HF) power, of 4.5% (-8.2 to -0.5) in the standard deviation of all normal-to-normal RR intervals (SDNN), of 10.6% (-18.5 to -1.9) in total power (TP) and an increase of 9.2% (0.8 to 20.2) in the LF/HF power ratio. CONCLUSIONS: In the absence of an overall effect our results suggest that alterations in HRV, a measure of autonomic control of the cardiac rhythm, may not be a central mechanism by which long-term exposure to TPM(10) increases cardiovascular mortality. Novel evidence on an effect in persons under ACE inhibitor treatment needs to be confirmed in future studie