Forest and Land Fires Are Mainly Associated with Deforestation in Riau Province, Indonesia

Indonesia has experienced extensive land-cover change and frequent vegetation and land fires in the past few decades. We combined a new land-cover dataset with satellite data on the timing and location of fires to make the first detailed assessment of the association of fire with specific land-cover transitions in Riau, Sumatra. During 1990 to 2017, secondary peat swamp forest declined in area from 40,000 to 10,000 km2 and plantations (including oil palm) increased from around 10,000 to 40,000 km2 . The dominant land use transitions were secondary peat swamp forest converting directly to plantation, or first to shrub and then to plantation. During 2001–2017, we find that the frequency of fire is greatest in regions that change land-cover, with the greatest frequency in regions that transition from secondary peat swamp forest to shrub or plantation (0.15 km−2 yr−1 ). Areas that did not change land cover exhibit lower fire frequency, with shrub (0.06 km−2 yr−1 ) exhibiting a frequency of fire >60 times the frequency of fire in primary forest. Our analysis demonstrates that in Riau, fire is closely connected to land-cover change, and that the majority of fire is associated with the transition of secondary forest to shrub and plantation. Reducing the frequency of fire in Riau will require enhanced protection of secondary forests and restoration of shrub to natural forest

Relationship Between Fire and Forest Cover Loss in Riau Province, Indonesia Between 2001 and 2012

Forest and peatland fires occur regularly across Indonesia, resulting in large greenhouse gas emissions and causing major air quality issues. Over the last few decades, Indonesia has also experienced extensive forest loss and conversion of natural forest to oil palm and timber plantations. Here we used data on fire hotspots and tree-cover loss, as well as information on the extent of peat land, protected areas, and concessions to explore spatial and temporal relationships among forest, forest loss, and fire frequency. We focus on the Riau Province in Central Sumatra, one of the most active regions of fire in Indonesia. We find strong relationships between forest loss and fire at the local scale. Regions with forest loss experienced six times as many fire hotspots compared to regions with no forest loss. Forest loss and maximum fire frequency occurred within the same year, or one year apart, in 70% of the 1 km2 cells experiencing both forest loss and fire. Frequency of fire was lower both before and after forest loss, suggesting that most fire is associated with the forest loss process. On peat soils, fire frequency was a factor 10 to 100 lower in protected areas and natural forest logging concessions compared to oil palm and wood fiber (timber) concessions. Efforts to reduce fire need to address the underlying role of land-use and land-cover change in the occurrence of fire. Increased support for protected areas and natural forest logging concessions and restoration of degraded peatlands may reduce future fire risk. During times of high fire risk, fire suppression resources should be targeted to regions that are experiencing recent forest loss, as these regions are most likely to experience fire

Assessing costs of Indonesian fires and the benefits of restoring peatland

Deforestation and drainage has made Indonesian peatlands susceptible to burning. Large fires occur regularly, destroying agricultural crops and forest, emitting large amounts of CO2 and air pollutants, resulting in adverse health effects. In order to reduce fire, the Indonesian government has committed to restore 2.49 Mha of degraded peatland, with an estimated cost of US$3.2-7 billion. Here we combine fire emissions and land cover data to estimate the 2015 fires, the largest in recent years, resulted in economic losses totalling US$28 billion, whilst the six largest fire events between 2004 and 2015 caused a total of US$93.9 billion in economic losses. We estimate that if restoration had already been completed, the area burned in 2015 would have been reduced by 6$8.4 billion for 2004–2015, making it a cost-effective strategy for reducing the impacts of peatland fires to the environment, climate and human health

Air quality and health impacts of vegetation and peat fires in Equatorial Asia during 2004–2015

Particulate matter (PM) emissions from vegetation and peat fires in Equatorial Asia cause poor regional air quality. Burning is greatest during drought years, resulting in strong inter-annual variability in emissions. We make the first consistent estimate of the emissions, air quality and public health impacts of Equatorial Asian fires during 2004–2015. The largest dry season (August—October) emissions occurred in 2015, with PM emissions estimated as 9.4 Tg, more than triple the average dry season emission (2.7 Tg). Fires in Sumatra and Kalimantan caused 94% of PM emissions from fires in Equatorial Asia. Peat combustion in Indonesian peatlands contributed 45% of PM emissions, with a greater contribution of 68% in 2015. We used the WRF-chem model to simulate dry season PM for the 6 biggest fire years during this period (2004, 2006, 2009, 2012, 2014, 2015). The model reproduces PM concentrations from a measurement network across Malaysia and Indonesia, suggesting our PM emissions are realistic. We estimate long-term exposure to PM resulted in 44 040 excess deaths in 2015, with more than 15 000 excess deaths annually in 2004, 2006, and 2009. Exposure to PM from dry season fires resulted in an estimated 131 700 excess deaths during 2004–2015. Our work highlights that Indonesian vegetation and peat fires frequently cause adverse impacts to public health across the region

Pooled sequencing of 531 genes in inflammatory bowel disease identifies an associated rare variant in BTNL2 and implicates other immune related genes.

The contribution of rare coding sequence variants to genetic susceptibility in complex disorders is an important but unresolved question. Most studies thus far have investigated a limited number of genes from regions which contain common disease associated variants. Here we investigate this in inflammatory bowel disease by sequencing the exons and proximal promoters of 531 genes selected from both genome-wide association studies and pathway analysis in pooled DNA panels from 474 cases of Crohn's disease and 480 controls. 80 variants with evidence of association in the sequencing experiment or with potential functional significance were selected for follow up genotyping in 6,507 IBD cases and 3,064 population controls. The top 5 disease associated variants were genotyped in an extension panel of 3,662 IBD cases and 3,639 controls, and tested for association in a combined analysis of 10,147 IBD cases and 7,008 controls. A rare coding variant p.G454C in the BTNL2 gene within the major histocompatibility complex was significantly associated with increased risk for IBD (p = 9.65x10-10, OR = 2.3[95% CI = 1.75-3.04]), but was independent of the known common associated CD and UC variants at this locus. Rare (T) or decreased risk (IL12B p.V298F, and NICN p.H191R) of IBD. These results provide additional insights into the involvement of the inhibition of T cell activation in the development of both sub-phenotypes of inflammatory bowel disease. We suggest that although rare coding variants may make a modest overall contribution to complex disease susceptibility, they can inform our understanding of the molecular pathways that contribute to pathogenesis

Autoimmune diseases - connecting risk alleles with molecular traits of the immune system

Genome-wide strategies have driven the discovery of more than 300 susceptibility loci for autoimmune diseases. However, for almost all loci, understanding of the mechanisms leading to autoimmunity remains limited, and most variants that are likely to be causal are in non-coding regions of the genome. A critical next step will be to identify the in vivo and ex vivo immunophenotypes that are affected by risk variants. To do this, key cell types and cell states that are implicated in autoimmune diseases will need to be defined. Functional genomic annotations from these cell types and states can then be used to resolve candidate genes and causal variants. Together with longitudinal studies, this approach may yield pivotal insights into how autoimmunity is triggered