Effect of short-term exposure to ambient nitrogen dioxide and particulate matter on repeated lung function measures in infancy: A South African birth cohort.

BACKGROUND: The developing lung is highly susceptible to environmental toxicants, with both short- and long-term exposure to ambient air pollutants linked to early childhood effects. This study assessed the short-term exposure effects of nitrogen dioxide (NO2) and particulate matter (PM10) on lung function in infants aged 6 weeks, 6, 12 and 24 months, the early developmental phase of child growth. METHODS: Lung function was determined by multiple breath washout and tidal breathing measurement in non-sedated infants. Individual exposure to NO2 and PM10 was determined by hybrid land use regression and dispersion modelling, with two-week average estimates (preceding the test date). Linear mixed models were used to adjust for the repeated measures design and an age*exposure interaction was introduced to obtain effect estimates for each age group. RESULTS: There were 165 infants that had lung function testing, with 82 of them having more than one test occasion. Exposure to PM10 (µg/m3) resulted in a decline in tidal volume at 6 weeks [-0.4 ml (-0.9; 0.0), p = 0.065], 6 months [-0.5 ml (-1.0; 0.0), p = 0.046] and 12 months [-0.3 ml (-0.7; 0.0), p = 0.045]. PM10 was related to an increase in respiratory rate and minute ventilation, while a decline was observed for functional residual capacity for the same age groups, though not statistically significant for these outcomes. Such associations were however less evident for exposure to NO2, with inconsistent changes observed across measurement parameters and age groups. CONCLUSION: Our study suggests that PM10 results in acute lung function impairments among infants from a low-socioeconomic setting, while the association with NO2 is less convincing.

Transcriptomic changes in the nasal epithelium associated with diesel engine exhaust exposure.

BACKGROUND: Diesel engine exhaust (DEE) exposure causes lung cancer, but the molecular mechanisms by which this occurs are not well understood. OBJECTIVES: To assess transcriptomic alterations in nasal epithelium of DEE-exposed factory workers to better understand the cellular and molecular effects of DEE. METHODS: Nasal epithelial brushings were obtained from 41 diesel engine factory workers exposed to relatively high levels of DEE (17.2-105.4 µg/m3), and 38 unexposed workers from factories without DEE exposure. mRNA was profiled for gene expression using Affymetrix microarrays. Linear modeling was used to identify differentially expressed genes associated with DEE exposure and interaction effects with current smoking status. Pathway enrichment among differentially expressed genes was assessed using EnrichR. Gene Set Enrichment Analysis (GSEA) was used to compare gene expression patterns between datasets. RESULTS: 225 genes had expression associated with DEE exposure after adjusting for smoking status (FDR q < 0.25) and were enriched for genes in pathways related to oxidative stress response, cell cycle pathways such as MAPK/ERK, protein modification, and transmembrane transport. Genes up-regulated in DEE-exposed individuals were enriched among the genes most up-regulated by cigarette smoking in a previously reported bronchial airway smoking dataset. We also found that the DEE signature was enriched among the genes most altered in two previous studies of the effects of acute DEE on PBMC gene expression. An exposure-response relationship was demonstrated between air levels of elemental carbon and the first principal component of the DEE signature. CONCLUSIONS: A gene expression signature was identified for workers occupationally exposed to DEE that was altered in an exposure-dependent manner and had some overlap with the effects of smoking and the effects of acute DEE exposure. This is the first study of gene expression in nasal epithelial cells of workers heavily exposed to DEE and provides new insights into the molecular alterations that occur with DEE exposure.

Particulate matter air pollution components and risk for lung cancer.

BACKGROUND: Particulate matter (PM) air pollution is a human lung carcinogen; however, the components responsible have not been identified. We assessed the associations between PM components and lung cancer incidence. METHODS: We used data from 14 cohort studies in eight European countries. We geocoded baseline addresses and assessed air pollution with land-use regression models for eight elements (Cu, Fe, K, Ni, S, Si, V and Zn) in size fractions of PM2.5 and PM10. We used Cox regression models with adjustment for potential confounders for cohort-specific analyses and random effect models for meta-analysis. RESULTS: The 245,782 cohort members contributed 3,229,220 person-years at risk. During follow-up (mean, 13.1 years), 1878 incident cases of lung cancer were diagnosed. In the meta-analyses, elevated hazard ratios (HRs) for lung cancer were associated with all elements except V; none was statistically significant. In analyses restricted to participants who did not change residence during follow-up, statistically significant associations were found for PM2.5 Cu (HR, 1.25; 95% CI, 1.01-1.53 per 5 ng/m(3)), PM10 Zn (1.28; 1.02-1.59 per 20 ng/m(3)), PM10 S (1.58; 1.03-2.44 per 200 ng/m(3)), PM10 Ni (1.59; 1.12-2.26 per 2 ng/m(3)) and PM10 K (1.17; 1.02-1.33 per 100 ng/m(3)). In two-pollutant models, associations between PM10 and PM2.5 and lung cancer were largely explained by PM2.5 S. CONCLUSIONS: This study indicates that the association between PM in air pollution and lung cancer can be attributed to various PM components and sources. PM containing S and Ni might be particularly important.

Performance of a high-volume cascade impactor in six European urban environments: mass measurement and chemical characterization of size-segregated particulate samples.

The performance of a modified Harvard high-volume cascade impactor (HVCI) was evaluated in six field campaigns with size-segregated particulate samplings for chemical and toxicological characterization. The 7-week sampling campaigns in 2002-2003 in Duisburg (autumn), Prague (winter), Amsterdam (winter), Helsinki (spring), Barcelona (spring), and Athens (summer) were selected to represent contrasting urban environments and seasons of public health interest due to high particulate concentrations or previous findings in epidemiological studies. Particulate samples were collected in parallel with the HVCI (PM(10-2.5), PM(2.5-1), PM(1-0.2), PM(0.2)), a virtual impactor (VI; PM(10-2.5), PM(2.5)), and a Berner low-pressure impactor (BLPI; 10 stages between 0.035 and 10 mum in particle diameter) using a 3- or 4-day sampling duration. The campaigns exhibited different profiles with regard to particulate mass concentration, size distribution, chemical composition and meteorological conditions, thus providing a demanding setup for an overall field comparison of the HVCI with the VI and BLPI reference samplers. Size-segregated particulate mass concentration could be reasonably well measured with the present HVCI configuration. The coarse (PM(10-2.5)) and fine (PM(2.5)) particulate mass agreed within 10% with the low-volume reference samplers, and the four-stage size distribution of the HVCI followed the modal pattern of urban aerosol. The concentrations of chemical constituents measured and integrated especially for the HVCI-PM(2.5) differed to some extent from those measured from the corresponding VI-PM(2.5) samples. This implies that when investigating the association of toxicological responses with the chemical constituents of particulate matter, it is necessary to use the chemical composition data of the same samples as used in toxicological experiments.