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BackgroundCommuters are exposed to high concentrations of air pollutants, but little quantitative information is currently available on differences in exposure between different modes of transport, routes, and fuel types.ObjectivesThe aim of our study was to assess differences in commuters’ exposure to traffic-related air pollution related to transport mode, route, and fuel type.MethodsWe measured particle number counts (PNCs) and concentrations of PM2.5 (particulate matter ≤ 2.5 μm in aerodynamic diameter), PM10, and soot between June 2007 and June 2008 on 47 weekdays, from 0800 to 1000 hours, in diesel and electric buses, gasoline- and diesel-fueled cars, and along two bicycle routes with different traffic intensities in Arnhem, the Netherlands. In addition, each-day measurements were taken at an urban background location.ResultsWe found that median PNC exposures were highest in diesel buses (38,500 particles/cm3) and for cyclists along the high-traffic intensity route (46,600 particles/cm3) and lowest in electric buses (29,200 particles/cm3). Median PM10 exposure was highest from diesel buses (47 μg/m3) and lowest along the high- and low-traffic bicycle routes (39 and 37 μg/m3). The median soot exposure was highest in gasoline-fueled cars (9.0 × 10−5/m), diesel cars (7.9 × 10−5/m), and diesel buses (7.4 × 10−5/m) and lowest along the low-traffic bicycle route (4.9 × 10−5/m). Because the minute ventilation (volume of air per minute) of cyclists, which we estimated from measured heart rates, was twice the minute ventilation of car and bus passengers, we calculated that the inhaled air pollution doses were highest for cyclists. With the exception of PM10, we found that inhaled air pollution doses were lowest for electric bus passengers.ConclusionsCommuters’ rush hour exposures were significantly influenced by mode of transport, route, and fuel type.

BackgroundSome legacy and emerging environmental contaminants are suspected risk factors for intrauterine growth restriction. However, the evidence is equivocal, in part due to difficulties in disentangling the effects of mixtures.ObjectivesWe assessed associations between multiple correlated biomarkers of environmental exposure and birth weight.MethodsWe evaluated a cohort of 1,250 term (≥ 37 weeks gestation) singleton infants, born to 513 mothers from Greenland, 180 from Poland, and 557 from Ukraine, who were recruited during antenatal care visits in 2002‒2004. Secondary metabolites of diethylhexyl and diisononyl phthalates (DEHP, DiNP), eight perfluoroalkyl acids, and organochlorines (PCB-153 and p,p´-DDE) were quantifiable in 72‒100% of maternal serum samples. We assessed associations between exposures and term birth weight, adjusting for co-exposures and covariates, including prepregnancy body mass index. To identify independent associations, we applied the elastic net penalty to linear regression models.ResultsTwo phthalate metabolites (MEHHP, MOiNP), perfluorooctanoic acid (PFOA), and p,p´-DDE were most consistently predictive of term birth weight based on elastic net penalty regression. In an adjusted, unpenalized regression model of the four exposures, 2-SD increases in natural log–transformed MEHHP, PFOA, and p,p´-DDE were associated with lower birth weight: –87 g (95% CI: –137, –340 per 1.70 ng/mL), –43 g (95% CI: –108, 23 per 1.18 ng/mL), and –135 g (95% CI: –192, –78 per 1.82 ng/g lipid), respectively; and MOiNP was associated with higher birth weight (46 g; 95% CI: –5, 97 per 2.22 ng/mL).ConclusionsThis study suggests that several of the environmental contaminants, belonging to three chemical classes, may be independently associated with impaired fetal growth. These results warrant follow-up in other cohorts.CitationLenters V, Portengen L, Rignell-Hydbom A, Jönsson BA, Lindh CH, Piersma AH, Toft G, Bonde JP, Heederik D, Rylander L, Vermeulen R. 2016. Prenatal phthalate, perfluoroalkyl acid, and organochlorine exposures and term birth weight in three birth cohorts: multi-pollutant models based on elastic net regression. Environ Health Perspect 124:365–372; http://dx.doi.org/10.1289/ehp.1408933

We found limited evidence to support a link between prenatal exposure to environmental chemical contaminants and childhood asthma and eczema.

Air pollution may accelerate arterial-wall stiffening in young adults. Small outcome variability and lack of residential mobility data may have limited the power to detect an effect on intima-media thickness.