Evidence for a role of long-term particulate matter exposure on acute respiratory infections is growing. However, which components of particulate matter may be causative remains largely unknown. We assessed associations between eight particulate matter elements and early-life pneumonia in seven birth cohort studies (Ntotal = 15,980): BAMSE (Sweden), GASPII (Italy), GINIplus and LISAplus (Germany), INMA (Spain), MAAS (United Kingdom) and PIAMA (The Netherlands). Annual average exposure to copper, iron, potassium, nickel, sulfur, silicon, vanadium and zinc, each respectively derived from particles with aerodynamic diameters ≤ 10 μm (PM10) and 2.5 μm (PM2.5), were estimated using standardized land use regression models and assigned to birth addresses. Cohort-specific associations between these exposures and parental reports of physician-diagnosed pneumonia between birth and two years were assessed using logistic regression models adjusted for host and environmental covariates and total PM10 or PM2.5 mass. Combined estimates were calculated using random-effects meta-analysis. There was substantial within and between-cohort variability in element concentrations. In the adjusted meta-analysis, pneumonia was weakly associated with zinc derived from PM10 (OR: 1.47 (95% CI: 0.99, 2.18) per 20 ng/m3 increase). No other associations with the other elements were consistently observed. The independent effect of particulate matter mass remained after adjustment for element concentrations. In conclusion, associations between particulate matter mass exposure and pneumonia were not explained by the elements we investigated. Zinc from PM10 was the only element which appeared independently associated with a higher risk of early-life pneumonia. As zinc is primarily attributable to non-tailpipe traffic emissions, these results may suggest a potential adverse effect of non-tailpipe emissions on health.

This research received funding from the European Community's Seventh Framework Program (FP7/2007-2011): ESCAPE (grant agreement number: 211250) and TRANSPHORM (ENV.2009.1.2.2.1). The Swedish Research Council FORMAS, the Stockholm County Council, the Swedish Foundation for Health Care Sciences and Allergy Research, and the Swedish Environmental Protection Agency supported BAMSE. The Italian Ministry of Health (ex art.12 D.Lgs 502/92, 2001) supported GASPII. The GINIplus study was supported for the first three years by grants of the Federal Ministry for Education, Science, Research and Technology (grant no. 01 EE 9401-4). The LISAplus study was supported by grants 01 EG 9732 and 01 EG 9705/2 from the Federal Ministry for Education, Science, Research and Technology, by the Federal Ministry for Environment (IUF, FKZ 20462296) and by the Helmholtz Zentrum München, Munich Center of Health. The Netherlands Organization for Health Research and Development, The Netherlands Organization for Scientific Research, The Netherlands Asthma Fund, The Netherlands Ministry of Spatial Planning, Housing, and the Environment and The Netherlands Ministry of Health, Welfare and Sport supported PIAMA. An Asthma UK Grant 04/014, the Moulton Charitable Trust, the James Trust and Microsoft Research supported MAAS. Grants from the Spanish Ministry of Health-Instituto de Salud Carlos III (Red INMA G03/176, CB06/02/0041, FISPI041436, FIS-PI081151, FIS-PI042018, FIS-PI09/02311, FIS-PI06/0867, FIS-PS09/00090, FIS-FEDER 03/1615, 04/1509, 04/1112, 04/1931, 05/1079, 05/1052, 06/1213, 07/0314, and 09/02647), Generalitat de Catalunya-CIRIT 1999SGR 00241, Conselleria de Sanitat Generalitat Valenciana, Universidad de Oviedo, Obra social Cajastur, Department of Health of the Basque Government (2005111093 and 2009111069), Provincial Government of Gipuzkoa (DFG06/004 and DFG08/001) and Fundación Roger Torné supported INMA.