May 27 | 2019

Association between exposure to the natural environment, rurality, and attention-deficit hyperactivity disorder in children in New Zealand: a linkage study.

Geoffrey H Donovan, PhD, Yvonne L Michael, ScD, Demetrios Gatziolis, PhD, Andrea ‘t Mannetje, PhD, Prof Jeroen Douwes, PhD

The Lancet Planetary Health Volume 3, Issue 5, May 2019, Pages e226-e234 DOI:



Several small experimental studies and cross-sectional observational studies have shown that exposure to the natural environment might protect against attention-deficit hyperactivity disorder (ADHD) or moderate the symptoms of ADHD in children. We aimed to assess whether exposure to the natural environment protects against ADHD and whether this hypothesised protective effect varies across a child’s life course.


We did a longitudinal study with data collected from all children born in New Zealand in 1998, excluding those without an address history, those who were not singleton births, and those who died or emigrated before 18 years of age. We used Statistics New Zealand’s Integrated Data Infrastructure to identify children with ADHD and to define covariates. ADHD was defined according to hospital diagnosis or pharmacy records (two or more prescriptions for ADHD drugs). Exposure to green space for each year of a child’s life (from gestation to 18 years of age) was estimated at the meshblock level (the smallest geographical unit for which the New Zealand Census reports data) using normalised difference vegetation index (NDVI), and land-use data from Landcare Research New Zealand. We used logit models to assess the associations between ADHD prevalence and minimum, maximum, and mean lifetime NDVI, as well as rural living, controlling for sex, ethnicity, mother’s educational level, mother’s smoking status, mother’s age at parturition, birth order, antibiotic use, and low birthweight.


Of the 57 450 children born in New Zealand in 1998, 49 923 were eligible and had available data, and were included in the analysis. Children who had always lived in a rural area after 2 years of age were less likely to develop ADHD (odds ratio [OR] 0·670 [95% CI 0·461–0·974), as were those with increased minimum NDVI exposure after age 2 years (standardised OR for exposure vs first quartile: second quartile 0·841 [0·707–0·999]; third quartile 0·809 [0·680–0·963]; fourth quartile 0·664 [0·548–0·805]). In early life (prenatal to age 2 years), neither rural living nor NDVI were protective against ADHD. Neither mean nor maximum greenness was significantly protective against ADHD.


Rurality and increased minimum greenness were strongly and independently associated with a reduced risk of ADHD. Increasing a child’s minimum lifetime greenness exposure, as opposed to maximum or mean exposure, might provide the greatest increment of protection against the disorder.

May 21 | 2019

Complex relationships between greenness, air pollution, and mortality in a population-based Canadian cohort.

Crouse DL, Pinault L, Balram A, Brauer M, Burnett RT, Martin RV, van Donkelaar A, Villeneuve PJ, Weichenthal S.

Environ Int. 2019 Jul;128:292-300. Epub 2019 May 7. DOI:10.1016/j.envint.2019.04.047



Epidemiological studies have consistently demonstrated that exposure to fine particulate matter (PM2.5) is associated with increased risks of mortality. To a lesser extent, a series of studies suggest that living in greener areas is associated with reduced risks of mortality. Only a handful of studies have examined the interplay between PM2.5, greenness, and mortality.


We investigated the role of residential greenness in modifying associations between long-term exposures to PM2.5 and non-accidental and cardiovascular mortality in a national cohort of non-immigrant Canadian adults (i.e., the 2001 Canadian Census Health and Environment Cohort). Specifically, we examined associations between satellite-derived estimates of PM2.5 exposure and mortality across quintiles of greenness measured within 500 m of individual’s place of residence during 11 years of follow-up. We adjusted our survival models for many personal and contextual measures of socioeconomic position, and residential mobility data allowed us to characterize annual changes in exposures.


Our cohort included approximately 2.4 million individuals at baseline, 194,270 of whom died from non-accidental causes during follow-up. Adjustment for greenness attenuated the association between PM2.5 and mortality (e.g., hazard ratios (HRs) and 95% confidence intervals (CIs) per interquartile range increase in PM2.5 in models for non-accidental mortality decreased from 1.065 (95% CI: 1.056-1.075) to 1.041 (95% CI: 1.031-1.050)). The strength of observed associations between PM2.5 and mortality decreased as greenness increased. This pattern persisted in models restricted to urban residents, in models that considered the combined oxidant capacity of ozone and nitrogen dioxide, and within neighbourhoods characterised by high or low deprivation. We found no increased risk of mortality associated with PM2.5among those living in the greenest areas. For example, the HR for cardiovascular mortality among individuals in the least green areas was 1.17 (95% CI: 1.12-1.23) compared to 1.01 (95% CI: 0.97-1.06) among those in the greenest areas.


Studies that do not account for greenness may overstate the air pollution impacts on mortality. Residents in deprived neighbourhoods with high greenness benefitted by having more attenuated associations between PM2.5 and mortality than those living in deprived areas with less greenness. The findings from this study extend our understanding of how living in greener areas may lead to improved health outcomes.

May 13 | 2019

Liveable for whom? Prospects of urban liveability to address health inequities.

Badland H, Pearce J.

Soc Sci Med. 2019 May 2;232:94-105. DOI: 10.1016/j.socscimed.2019.05.001


The aspiration of liveable cities, underpinned by the New Urban Agenda, is gaining popularity as a mechanism to enhance population health and wellbeing. However, less attention has been given to understanding how urban liveability may provide an opportunity to redress health inequities. Using an environmental justice lens, this paper investigates whether urban liveability poses an opportunity or threat to reducing health inequities and outlines a future research agenda. Selected urban liveability attributes, being: education; employment; food, alcohol, and tobacco; green space; housing; transport; and walkability, were investigated to understand how they can serve to widen or narrow inequities. Some domains showed consistent evidence, others suggested context-specific associations that made it difficult to draw general conclusions, and some showed a reverse patterning with the social gradient, but with poorer outcomes. This suggests urban liveability attributes have equigenic potential, but operate within a complex system. We conclude more disadvantaged neighbourhoods and their residents likely have additional policy and design considerations for optimising outcomes, especially as changes to the contextual environment may impact neighbourhood composition through displacement and/or pulling up effects. Future research needs to continue to explore downstream associations using longitudinal and natural experiments, and also seek to gain a deeper understanding of the urban liveability system, including interactions, feedback loops, and non-linear and linear responses. There is a need to monitor neighbourhood population changes over time to understand how liveability impacts the most vulnerable. Other areas worthy of further investigation include applying a life course approach and understanding liveability within the context of other adversities and contextual settings.

May 6 | 2019

Early-life exposome and lung function in children in Europe: an analysis of data from the longitudinal, population-based HELIX cohort.

Agier L, Basagaña X, Maitre L, Granum B, Bird PK, Casas M, Oftedal B, Wright J, Andrusaityte S, de Castro M, Cequier E, Chatzi L, Donaire-Gonzalez D, Grazuleviciene R, Haug LS, Sakhi AK, Leventakou V, McEachan R, Nieuwenhuijsen M, Petraviciene I, Robinson O, Roumeliotaki T, Sunyer J, Tamayo-Uria I, Thomsen C, Urquiza J, Valentin A, Slama R, Vrijheid M, Siroux V.

Lancet Planet Health. 2019 Feb;3 (2):e81-e92.



Several single-exposure studies have documented possible effects of environmental factors on lung function, but none has relied on an exposome approach. We aimed to evaluate the association between a broad range of prenatal and postnatal lifestyle and environmental exposures and lung function in children.


In this analysis, we used data from 1033 mother-child pairs from the European Human Early-Life Exposome (HELIX) cohort (consisting of six existing longitudinal birth cohorts in France, Greece, Lithuania, Norway, Spain, and the UK of children born between 2003 and 2009) for whom a valid spirometry test was recorded for the child. 85 prenatal and 125 postnatal exposures relating to outdoor, indoor, chemical, and lifestyle factors were assessed, and lung function was measured by spirometry in children at age 6-12 years. Two agnostic linear regression methods, a deletion-substitution-addition (DSA) algorithm considering all exposures simultaneously, and an exposome-wide association study (ExWAS) considering exposures independently, were applied to test the association with forced expiratory volume in 1 s percent predicted values (FEV1%). We tested for two-way interaction between exposures and corrected for confounding by co-exposures.


In the 1033 children (median age 8·1 years, IQR 6·5-9·0), mean FEV1% was 98·8% (SD 13·2). In the ExWAS, prenatal perfluorononanoate (p=0·034) and perfluorooctanoate (p=0·030) exposures were associated with lower FEV1%, and inverse distance to nearest road during pregnancy (p=0·030) was associated with higher FEV1%. Nine postnatal exposures were associated with lower FEV1%: copper (p=0·041), ethyl-paraben (p=0·029), five phthalate metabolites (mono-2-ethyl 5-carboxypentyl phthalate [p=0·016], mono-2-ethyl-5-hydroxyhexyl phthalate [p=0·023], mono-2-ethyl-5-oxohexyl phthalate [p=0·0085], mono-4-methyl-7-oxooctyl phthalate [p=0·040], and the sum of di-ethylhexyl phthalate metabolites [p=0·014]), house crowding (p=0·015), and facility density around schools (p=0·027). However, no exposure passed the significance threshold when corrected for multiple testing in ExWAS, and none was selected with the DSA algorithm, including when testing for exposure interactions.


Our systematic exposome approach identified several environmental exposures, mainly chemicals, that might be associated with lung function. Reducing exposure to these ubiquitous chemicals could help to prevent the development of chronic respiratory disease.