Early-life environmental exposures and blood pressure in children

Background: Growing evidence exists about the fetal and environmental origins of hypertension, but mainly limited to single-exposure studies. The exposome has been proposed as a more holistic approach by studying many exposures simultaneously. Objectives: This study aims to evaluate the association between a wide range of prenatal and postnatal exposures and blood pressure (BP) in children. Methods: Systolic and diastolic BP were measured among 1,277 children from the European HELIX (Human Early-Life Exposome) cohort aged 6 to 11 years. Prenatal (n = 89) and postnatal (n = 128) exposures include air pollution, built environment, meteorology, natural spaces, traffic, noise, chemicals, and lifestyles. Two methods adjusted for confounders were applied: an exposome-wide association study considering the exposures independently, and the deletion-substitution-addition algorithm considering all the exposures simultaneously. Results: Decreases in systolic BP were observed with facility density (β change for an interquartile-range increase in exposure: −1.7 mm Hg [95% confidence interval (CI): −2.5 to −0.8 mm Hg]), maternal concentrations of polychlorinated biphenyl 118 (−1.4 mm Hg [95% CI: −2.6 to −0.2 mm Hg]) and child concentrations of dichlorodiphenyldichloroethylene (DDE: −1.6 mm Hg [95% CI: −2.4 to −0.7 mm Hg]), hexachlorobenzene (−1.5 mm Hg [95% CI: −2.4 to −0.6 mm Hg]), and mono−benzyl phthalate (−0.7 mm Hg [95% CI: −1.3 to −0.1 mm Hg]), whereas increases in systolic BP were observed with outdoor temperature during pregnancy (1.6 mm Hg [95% CI: 0.2 to 2.9 mm Hg]), high fish intake during pregnancy (2.0 mm Hg [95% CI: 0.4 to 3.5 mm Hg]), maternal cotinine concentrations (1.2 mm Hg [95% CI: -0.3 to 2.8 mm Hg]), and child perfluorooctanoate concentrations (0.9 mm Hg [95% CI: 0.1 to 1.6 mm Hg]). Decreases in diastolic BP were observed with outdoor temperature at examination (−1.4 mm Hg [95% CI: −2.3 to −0.5 mm Hg]) and child DDE concentrations (−1.1 mm Hg [95% CI: −1.9 to −0.3 mm Hg]), whereas increases in diastolic BP were observed with maternal bisphenol-A concentrations (0.7 mm Hg [95% CI: 0.1 to 1.4 mm Hg]), high fish intake during pregnancy (1.2 mm Hg [95% CI: −0.2 to 2.7 mm Hg]), and child copper concentrations (0.9 mm Hg [95% CI: 0.3 to 1.6 mm Hg]). Conclusions: This study suggests that early-life exposure to several chemicals, as well as built environment and meteorological factors, may affect BP in children

Is there an association between ambient air pollution and bladder cancer incidence – Analysis of 15 European cohorts?

Background Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer. Little is known about whether exposure to air pollution influences bladder cancer in the general population. Objective We aimed to evaluate the association between long-term exposure to ambient air pollution and bladder cancer incidence. Design, setting and participants We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303,431; mean follow-up 14.1 years). We estimated exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter &lt;10μm (PM10), &lt;2.5 μm (PM2.5), between 2.5 and 10 μm (PM2.5-10), PM2.5 absorbance (soot), elemental constituents of PM, organic carbon and traffic density at baseline home addresses using standardized land-use regression models from the ESCAPE (European Study of Cohorts for Air Pollution Effects) project. Outcome measurements and statistical analysis We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for bladder cancer incidence. Results and Limitations During follow-up, 943 incident bladder cancer cases were diagnosed. In the meta-analysis, none of the exposures were associated with bladder cancer risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval (CI): 0.89, 1.08) and 0.86 (95%CI: 0.63, 1.18), respectively. Limitations include lack of information about lifetime exposure. Conclusion There was no evidence of an association between exposure to outdoor air pollution levels at residence and risk of bladder cancer. Patient summary We assessed the link between outdoor air pollution at residence and bladder cancer, using the largest study population to date, extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at residence and bladder cancer risk.1</p

Air pollution and incidence of cancers of the stomach and the upper aerodigestive tract in the European Study of Cohorts for Air Pollution Effects (ESCAPE)

Air pollution has been classified as carcinogenic to humans. However, to date little is known about the relevance for cancers of the stomach and upper aerodigestive tract (UADT). We investigated the association of long‐term exposure to ambient air pollution with incidence of gastric and UADT cancer in 11 European cohorts. Air pollution exposure was assigned by land‐use regression models for particulate matter (PM) below 10 µm (PM10), below 2.5 µm (PM2.5), between 2.5 and 10 µm (PMcoarse), PM2.5 absorbance and nitrogen oxides (NO2 and NOX) as well as approximated by traffic indicators. Cox regression models with adjustment for potential confounders were used for cohort‐specific analyses. Combined estimates were determined with random effects meta‐analyses. During average follow‐up of 14.1 years of 305,551 individuals, 744 incident cases of gastric cancer and 933 of UADT cancer occurred. The hazard ratio for an increase of 5 µg/m3 of PM2.5 was 1.38 (95% CI 0.99; 1.92) for gastric and 1.05 (95% CI 0.62; 1.77) for UADT cancers. No associations were found for any of the other exposures considered. Adjustment for additional confounders and restriction to study participants with stable addresses did not influence markedly the effect estimate for PM2.5 and gastric cancer. Higher estimated risks of gastric cancer associated with PM2.5 was found in men (HR 1.98 [1.30; 3.01]) as compared to women (HR 0.85 [0.5; 1.45]). This large multicentre cohort study shows an association between long‐term exposure to PM2.5 and gastric cancer, but not UADT cancers, suggesting that air pollution may contribute to gastric cancer risk

Is there an association between ambient air pollution and bladder cancer incidence – Analysis of 15 European cohorts?

Background Ambient air pollution contains low concentrations of carcinogens implicated in the etiology of urinary bladder cancer. Little is known about whether exposure to air pollution influences bladder cancer in the general population. Objective We aimed to evaluate the association between long-term exposure to ambient air pollution and bladder cancer incidence. Design, setting and participants We obtained data from 15 population-based cohorts enrolled between 1985 and 2005 in eight European countries (N=303,431; mean follow-up 14.1 years). We estimated exposure to nitrogen oxides (NO2 and NOX), particulate matter (PM) with diameter Outcome measurements and statistical analysis We used Cox proportional-hazards models with adjustment for potential confounders for cohort-specific analyses and meta-analyses to estimate summary hazard ratios (HRs) for bladder cancer incidence. Results and Limitations During follow-up, 943 incident bladder cancer cases were diagnosed. In the meta-analysis, none of the exposures were associated with bladder cancer risk. The summary HRs associated with a 10-μg/m3 increase in NO2 and 5-μg/m3 increase in PM2.5 were 0.98 (95% confidence interval (CI): 0.89, 1.08) and 0.86 (95%CI: 0.63, 1.18), respectively. Limitations include lack of information about lifetime exposure. Conclusion There was no evidence of an association between exposure to outdoor air pollution levels at residence and risk of bladder cancer. Patient summary We assessed the link between outdoor air pollution at residence and bladder cancer, using the largest study population to date, extensive assessment of exposure and comprehensive data on personal risk factors such as smoking. We found no association between the levels of outdoor air pollution at residence and bladder cancer risk.1</p